Author: "Olivier Disson" - Searchworks@Jio Institute Digital Library Search Results

Your search keyword '"Olivier Disson"' showing total 60 results

Start Over Author "Olivier Disson"

60 results on '"Olivier Disson"'

1. Protocol for live imaging of bacteria-cell interactions in genetically modified mouse small intestinal organoids

Author: Minhee Kim, Cindy Fèvre, Morgane Lavina, Olivier Disson, and Marc Lecuit
Subjects: Cell Biology, Microbiology, Microscopy, Organoids, Tissue Engineering, Science (General), Q1-390
Abstract: Summary: Here, we present a protocol for microinjection of bacteria into mouse small intestinal organoids that recapitulates the natural route of infection of intestinal epithelial cells from the intestinal lumen. We describe steps for visualizing bacteria-cell interactions by live imaging of infected organoids using light sheet microscopy. We then detail procedures for generating doxycycline-inducible expression of mutant proteins in organoids to study essential gene functions. The different techniques described in this protocol can be used independently as required.For complete details on the use and execution of this protocol, please refer to Kim et al. (2021).1 : Publisher’s note: Undertaking any experimental protocol requires adherence to local institutional guidelines for laboratory safety and ethics.
Published: 2024
Full Text: View/download PDF

2. Maternal-neonatal listeriosis

Author: Caroline Charlier, Olivier Disson, and Marc Lecuit
Subjects: listeriosis, listeria monocytogenes, placenta, pregnancy, newborn, fetus, infection, Infectious and parasitic diseases, RC109-216
Abstract: Listeriosis is a rare and severe foodborne infection caused by Listeria monocytogenes. It manifests as septicemia, neurolisteriosis, and maternal-fetal infection. In pregnancy, it may cause maternal fever, premature delivery, fetal loss, neonatal systemic and central nervous system infections. Maternal listeriosis is mostly reported during the 2nd and 3rd trimester of pregnancy, as sporadic cases or in the context of outbreaks. Strains belonging to clonal complexes 1, 4 and 6, referred to as hypervirulent, are the most associated to maternal-neonatal infections. Here we review the clinical, pathophysiological, and microbiological features of maternal-neonatal listeriosis.
Published: 2020
Full Text: View/download PDF

3. Neonatal susceptibility to meningitis results from the immaturity of epithelial barriers and gut microbiota

Author: Laetitia Travier, Mariana Alonso, Alessio Andronico, Lukas Hafner, Olivier Disson, Pierre-Marie Lledo, Simon Cauchemez, and Marc Lecuit
Subjects: infection, intestine, neonatal, meningitis, choroid plexus, intestinal barrier, Biology (General), QH301-705.5
Abstract: Summary: Neonates are highly susceptible to bacterial meningitis as compared to children and adults. Group B streptococcus (GBS) is a major cause of neonatal meningitis. Neonatal meningitis can result from GBS intestinal colonization and translocation across the intestinal barrier (IB). Here, we show that the immaturity of the neonatal intestinal microbiota leads to low resistance to GBS intestinal colonization and permissiveness of the gut-vascular barrier. Moreover, the age-dependent but microbiota-independent Wnt activity in intestinal and choroid plexus (CP) epithelia results in a lower degree of cell-cell junctions’ polarization, which favors bacterial translocation. This study thus reveals that neonatal susceptibility to GBS meningitis results from the age-dependent immaturity of the intestinal microbiota and developmental pathways associated with neonatal tissue growth, which both concur to GBS gut colonization, systemic dissemination, and neuroinvasion. Whereas the activation of developmental pathways is intrinsic to neonates, interventions aimed at maturing the microbiota may help prevent neonatal meningitis.
Published: 2021
Full Text: View/download PDF

4. Hypervirulent Listeria monocytogenes clones’ adaption to mammalian gut accounts for their association with dairy products

Author: Mylène M. Maury, Hélène Bracq-Dieye, Lei Huang, Guillaume Vales, Morgane Lavina, Pierre Thouvenot, Olivier Disson, Alexandre Leclercq, Sylvain Brisse, and Marc Lecuit
Subjects: Science
Abstract: Here, Maury et al. show that hypervirulent Listeria monocytogenes (Lm) clones associated to dairy products exhibit higher adaptation to the mammalian gut environment, while hypovirulent clones persist in food processing environment, suggesting a relationship between Lm pathogenic potential and niche adaptation.
Published: 2019
Full Text: View/download PDF

5. Phage resistance at the cost of virulence: Listeria monocytogenes serovar 4b requires galactosylated teichoic acids for InlB-mediated invasion.

Author: Eric T Sumrall, Yang Shen, Anja P Keller, Jeanine Rismondo, Maria Pavlou, Marcel R Eugster, Samy Boulos, Olivier Disson, Pierre Thouvenot, Samuel Kilcher, Bernd Wollscheid, Didier Cabanes, Marc Lecuit, Angelika Gründling, and Martin J Loessner
Subjects: Immunologic diseases. Allergy, RC581-607, Biology (General), QH301-705.5
Abstract: The intracellular pathogen Listeria monocytogenes is distinguished by its ability to invade and replicate within mammalian cells. Remarkably, of the 15 serovars within the genus, strains belonging to serovar 4b cause the majority of listeriosis clinical cases and outbreaks. The Listeria O-antigens are defined by subtle structural differences amongst the peptidoglycan-associated wall-teichoic acids (WTAs), and their specific glycosylation patterns. Here, we outline the genetic determinants required for WTA decoration in serovar 4b L. monocytogenes, and demonstrate the exact nature of the 4b-specific antigen. We show that challenge by bacteriophages selects for surviving clones that feature mutations in genes involved in teichoic acid glycosylation, leading to a loss of galactose from both wall teichoic acid and lipoteichoic acid molecules, and a switch from serovar 4b to 4d. Surprisingly, loss of this galactose decoration not only prevents phage adsorption, but leads to a complete loss of surface-associated Internalin B (InlB),the inability to form actin tails, and a virulence attenuation in vivo. We show that InlB specifically recognizes and attaches to galactosylated teichoic acid polymers, and is secreted upon loss of this modification, leading to a drastically reduced cellular invasiveness. Consequently, these phage-insensitive bacteria are unable to interact with cMet and gC1q-R host cell receptors, which normally trigger cellular uptake upon interaction with InlB. Collectively, we provide detailed mechanistic insight into the dual role of a surface antigen crucial for both phage adsorption and cellular invasiveness, demonstrating a trade-off between phage resistance and virulence in this opportunistic pathogen.
Published: 2019
Full Text: View/download PDF

6. Author Correction: Hypervirulent Listeria monocytogenes clones’ adaptation to mammalian gut accounts for their association with dairy products

Author: Mylène M. Maury, Hélène Bracq-Dieye, Lei Huang, Guillaume Vales, Morgane Lavina, Pierre Thouvenot, Olivier Disson, Alexandre Leclercq, Sylvain Brisse, and Marc Lecuit
Subjects: Science
Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper.
Published: 2019
Full Text: View/download PDF

7. Human Listeriosis Caused by Listeria ivanovii

Author: Christelle Guillet, Olivier Join-Lambert, Alban Le Monnier, Alexandre Leclercq, Frédéric Mechaï, Marie-France Mamzer-Bruneel, Magdalena K. Bielecka, Mariela Scortti, Olivier Disson, Patrick Berche, José Vazquez-Boland, Olivier Lortholary, and Marc Lecuit
Subjects: Listeria ivanovii, gastroenteritis, bacteremia, kidney transplantation, bacteria, dispatch, Medicine, Infectious and parasitic diseases, RC109-216
Abstract: Two species of Listeria are pathogenic; L. monocytogenes infects humans and animals, and L. ivanovii has been considered to infect ruminants only. We report L. ivanovii–associated gastroenteritis and bacteremia in a man. This isolate was indistinguishable from prototypic ruminant strains. L. ivanovii is thus an enteric opportunistic human pathogen.
Published: 2010
Full Text: View/download PDF

8. ActA promotes Listeria monocytogenes aggregation, intestinal colonization and carriage.

Author: Laetitia Travier, Stéphanie Guadagnini, Edith Gouin, Alexandre Dufour, Viviane Chenal-Francisque, Pascale Cossart, Jean-Christophe Olivo-Marin, Jean-Marc Ghigo, Olivier Disson, and Marc Lecuit
Subjects: Immunologic diseases. Allergy, RC581-607, Biology (General), QH301-705.5
Abstract: Listeria monocytogenes (Lm) is a ubiquitous bacterium able to survive and thrive within the environment and readily colonizes a wide range of substrates, often as a biofilm. It is also a facultative intracellular pathogen, which actively invades diverse hosts and induces listeriosis. So far, these two complementary facets of Lm biology have been studied independently. Here we demonstrate that the major Lm virulence determinant ActA, a PrfA-regulated gene product enabling actin polymerization and thereby promoting its intracellular motility and cell-to-cell spread, is critical for bacterial aggregation and biofilm formation. We show that ActA mediates Lm aggregation via direct ActA-ActA interactions and that the ActA C-terminal region, which is not involved in actin polymerization, is essential for aggregation in vitro. In mice permissive to orally-acquired listeriosis, ActA-mediated Lm aggregation is not observed in infected tissues but occurs in the gut lumen. Strikingly, ActA-dependent aggregating bacteria exhibit an increased ability to persist within the cecum and colon lumen of mice, and are shed in the feces three order of magnitude more efficiently and for twice as long than bacteria unable to aggregate. In conclusion, this study identifies a novel function for ActA and illustrates that in addition to contributing to its dissemination within the host, ActA plays a key role in Lm persistence within the host and in transmission from the host back to the environment.
Published: 2013
Full Text: View/download PDF

9. Murinization of internalin extends its receptor repertoire, altering Listeria monocytogenes cell tropism and host responses.

Author: Yu-Huan Tsai, Olivier Disson, Hélène Bierne, and Marc Lecuit
Subjects: Immunologic diseases. Allergy, RC581-607, Biology (General), QH301-705.5
Abstract: Listeria monocytogenes (Lm) is an invasive foodborne pathogen that leads to severe central nervous system and maternal-fetal infections. Lm ability to actively cross the intestinal barrier is one of its key pathogenic properties. Lm crosses the intestinal epithelium upon the interaction of its surface protein internalin (InlA) with its host receptor E-cadherin (Ecad). InlA-Ecad interaction is species-specific, does not occur in wild-type mice, but does in transgenic mice expressing human Ecad and knock-in mice expressing humanized mouse Ecad. To study listeriosis in wild-type mice, InlA has been "murinized" to interact with mouse Ecad. Here, we demonstrate that, unexpectedly, murinized InlA (InlA(m)) mediates not only Ecad-dependent internalization, but also N-cadherin-dependent internalization. Consequently, InlA(m)-expressing Lm targets not only goblet cells expressing luminally-accessible Ecad, as does Lm in humanized mice, but also targets villous M cells, which express luminally-accessible N-cadherin. This aberrant Lm portal of entry results in enhanced innate immune responses and intestinal barrier damage, both of which are not observed in wild-type Lm-infected humanized mice. Murinization of InlA therefore not only extends the host range of Lm, but also broadens its receptor repertoire, providing Lm with artifactual pathogenic properties. These results challenge the relevance of using InlA(m)-expressing Lm to study human listeriosis and in vivo host responses to this human pathogen.
Published: 2013
Full Text: View/download PDF

10. A mouse model for Chikungunya: young age and inefficient type-I interferon signaling are risk factors for severe disease.

Author: Thérèse Couderc, Fabrice Chrétien, Clémentine Schilte, Olivier Disson, Madly Brigitte, Florence Guivel-Benhassine, Yasmina Touret, Georges Barau, Nadège Cayet, Isabelle Schuffenecker, Philippe Desprès, Fernando Arenzana-Seisdedos, Alain Michault, Matthew L Albert, and Marc Lecuit
Subjects: Immunologic diseases. Allergy, RC581-607, Biology (General), QH301-705.5
Abstract: Chikungunya virus (CHIKV) is a re-emerging arbovirus responsible for a massive outbreak currently afflicting the Indian Ocean region and India. Infection from CHIKV typically induces a mild disease in humans, characterized by fever, myalgia, arthralgia, and rash. Cases of severe CHIKV infection involving the central nervous system (CNS) have recently been described in neonates as well as in adults with underlying conditions. The pathophysiology of CHIKV infection and the basis for disease severity are unknown. To address these critical issues, we have developed an animal model of CHIKV infection. We show here that whereas wild type (WT) adult mice are resistant to CHIKV infection, WT mouse neonates are susceptible and neonatal disease severity is age-dependent. Adult mice with a partially (IFN-alpha/betaR(+/-)) or totally (IFN-alpha/betaR(-/-)) abrogated type-I IFN pathway develop a mild or severe infection, respectively. In mice with a mild infection, after a burst of viral replication in the liver, CHIKV primarily targets muscle, joint, and skin fibroblasts, a cell and tissue tropism similar to that observed in biopsy samples of CHIKV-infected humans. In case of severe infections, CHIKV also disseminates to other tissues including the CNS, where it specifically targets the choroid plexuses and the leptomeninges. Together, these data indicate that CHIKV-associated symptoms match viral tissue and cell tropisms, and demonstrate that the fibroblast is a predominant target cell of CHIKV. These data also identify the neonatal phase and inefficient type-I IFN signaling as risk factors for severe CHIKV-associated disease. The development of a permissive small animal model will expedite the testing of future vaccines and therapeutic candidates.
Published: 2008
Full Text: View/download PDF

11. Listeriosis, a model infection to study host-pathogen interactions in vivo

Author: Hana Kammoun, Minhee Kim, Lukas Hafner, Julien Gaillard, Olivier Disson, and Marc Lecuit
Subjects: Microbiology (medical), Infectious Diseases, Bacterial Proteins, Pregnancy, Placenta, Host-Pathogen Interactions, Animals, Female, Listeriosis, Listeria monocytogenes, Microbiology
Abstract: Listeria monocytogenes (Lm) is a foodborne pathogen and the etiological agent of listeriosis. This facultative intracellular Gram-positive bacterium has the ability to colonize the intestinal lumen, cross the intestinal, blood-brain and placental barriers, leading to bacteremia, neurolisteriosis and maternal-fetal listeriosis. Lm is a model microorganism for the study of the interplay between a pathogenic microbe, host tissues and microbiota in vivo. Here we review how animal models permissive to Lm-host interactions allow deciphering some of the key steps of the infectious process, from the intestinal lumen to the crossing of host barriers and dissemination within the host. We also highlight recent investigations using tagged Lm and clinically relevant strains that have shed light on within-host dynamics and the purifying selection of Lm virulence factors. Studying Lm infection in vivo is a way forward to explore host biology and unveil the mechanisms that have selected its capacity to closely associate with its vertebrate hosts.
Published: 2022

12. Microbiota-induced active translocation of peptidoglycan across the intestinal barrier dictates its within-host dissemination

Author: Richard Wheeler, Paulo André Dias Bastos, Olivier Disson, Aline Rifflet, Ilana Gabanyi, Julia Spielbauer, Marion Bérard, Marc Lecuit, Ivo Gomperts Boneca, Biologie et Génétique de la Paroi bactérienne - Biology and Genetics of Bacterial Cell Wall, Institut Pasteur [Paris] (IP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité)-Microbiologie Intégrative et Moléculaire (UMR6047), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Biologie des Infections - Biology of Infection, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Perception et Mémoire / Perception and Memory, Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Microenvironnement et Immunité - Microenvironment and Immunity, Animalerie Centrale (plateforme) - Central Animal Facility (platform) (C2RA), Institut Pasteur [Paris] (IP)-Université Paris Cité (UPCité), Centre National de Référence Listeria - National Reference Center Listeria (CNR), Centre collaborateur de l'OMS Listeria / WHO Collaborating Centre Listeria (CC-OMS / WHO-CC), Institut Pasteur [Paris] (IP)-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO)-Université Paris Cité (UPCité), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), This project has received funding from the Institut Carnot Pasteur Microbes & Santé, and the European Union's Horizon 2020 research and innovation program under the Marie Sklodowska-Curie grant agreement no 665807. A.R. and I.G.B. laboratory were supported by Investissement d’Avenir program, Laboratoire d’Excellence 'Integrative Biology of Emerging Infectious Diseases' (ANR-10-LABX-62-IBEID). I.G.B. laboratory was also supported by the Investissement d’Avenir program (RHU Torino Lumière ANR-16-RHUS-0008), by the French National Research Agency (ANR-16-CE15-0021) and by R&D grants from Danone and MEIJI. Additional funding was provided by DIM1Health., We thank the UTechS PBI, a member of the France–BioImaging infrastructure network supported by the French National Research Agency (ANR-10–INSB–04, Investments for the future) for microscope usage and assistance. We thank the members of the Centre for Gnotobiology Platform of the Institut Pasteur (especially Thierry Angélique, Eddie Maranghi, Martine Jacob, and Marisa Gabriela Lopez Dieguez), and of the Institut Pasteur Central Animal Facility for all their assistance with animal studies. P.A.D.B. was part of the Pasteur-Paris University International PhD Program., ANR-10-LABX-0062,IBEID,Integrative Biology of Emerging Infectious Diseases(2010), ANR-10-INBS-0004,France-BioImaging,Développment d'une infrastructure française distribuée coordonnée(2010), ANR-16-RHUS-0008,LUMIERE,LUMIERE(2016), ANR-16-CE15-0021,PG-Brain,Modulation de l'activité du cerveau par le peptidoglycan bactérien(2016), and European Project: 665807,H2020,H2020-MSCA-COFUND-2014,PASTEURDOC(2015)
Subjects: Multidisciplinary, gut microbiota, systemic trafficking, [SDV.BA]Life Sciences [q-bio]/Animal biology, [SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, [SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], peptidoglycan, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology
Abstract: International audience; Peptidoglycan, the major structural polymer forming the cell wall of bacteria, is an important mediator of physiological and behavioral effects in mammalian hosts. These effects are frequently linked to its translocation from the intestinal lumen to host tissues. However, the modality and regulation of this translocation across the gut barrier has not been precisely addressed. In this study, we characterized the absorption of peptidoglycan across the intestine and its systemic dissemination. We report that peptidoglycan has a distinct tropism for host organs when absorbed via the gut, most notably by favoring access to the brain. We demonstrate that intestinal translocation of peptidoglycan occurs through a microbiota-induced active process. This process is regulated by the parasympathetic pathway via the muscarinic acetylcholine receptors. Together, this study reveals fundamental parameters concerning the uptake of a major microbiota molecular signal from the steady-state gut.
Published: 2023

13. Usp22 is an intracellular regulator of systemic emergency hematopoiesis

Author: Nikolaus Dietlein, Xi Wang, Jonas Metz, Olivier Disson, Fuwei Shang, Celine Beyersdörffer, Esther Rodríguez Correa, Daniel B. Lipka, Yvonne Begus-Nahrmann, Robyn Laura Kosinsky, Steven A. Johnsen, Marc Lecuit, Thomas Höfer, Hans-Reimer Rodewald, German Cancer Research Center - Deutsches Krebsforschungszentrum [Heidelberg] (DKFZ), Universität Heidelberg [Heidelberg] = Heidelberg University, Nanjing Medical University, Biologie des Infections - Biology of Infection, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Otto-von-Guericke-Universität Magdeburg = Otto-von-Guericke University [Magdeburg] (OVGU), University Medical Center Göttingen (UMG), Mayo Clinic [Rochester], Robert Bosch Centre for Tumor Diseases [Stuttgart, Germany] (RBCT), Centre National de Référence Listeria - National Reference Center Listeria (CNR), Centre collaborateur de l'OMS Listeria / WHO Collaborating Centre Listeria (CC-OMS / WHO-CC), Institut Pasteur [Paris] (IP)-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO)-Université Paris Cité (UPCité), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), N.D. was supported by a Helmholtz Graduate School for Cancer Research fellowship, D.B.L. was supported by Deutsche Krebshilfe Grant 70112574, M.L. and O.D. were supported by Institut Pasteur and Inserm core funding, H.-R.R. and T.H. were supported by Sonderforschungsbereich (SFB) 873-B11, and and H.-R.R. was supported by the European Research Council Advanced Grant 742883, the Helmholtz I & I Initiative program, and the Leibniz program of the Deutsche Forschungsgemeinschaft.
Subjects: [SDV]Life Sciences [q-bio], Immunology, [SDV.IMM]Life Sciences [q-bio]/Immunology, General Medicine
Abstract: Emergency hematopoiesis is a concerted response aimed toward enhanced protection from infection, involving multiple cell types and developmental stages across the immune system. Despite its importance, the underlying molecular regulation remains poorly understood. The deubiquitinase USP22 regulates the levels of monoubiquitinated histone H2B (H2Bub1), which is associated with activation of interferon responses upon viral infection. Here, we show that in the absence of infection or inflammation, mice lacking Usp22 in all hematopoietic cells display profound systemic emergency hematopoiesis, evident by increased hematopoietic stem cell proliferation, myeloid bias, and extramedullary hematopoiesis. Functionally, loss of Usp22 results in elevated phagocytosis by neutrophilic granulocytes and enhanced innate protection against Listeria monocytogenes infection. At the molecular level, we found this state of emergency hematopoiesis associated with transcriptional signatures of myeloid priming, enhanced mitochondrial respiration, and innate and adaptive immunity and inflammation. Augmented expression of many inflammatory genes was linked to elevated locus-specific H2Bub1 levels. Collectively, these results demonstrate the existence of a tunable epigenetic state that promotes systemic emergency hematopoiesis in a cell-autonomous manner to enhance innate protection, identifying potential paths toward immune enhancement.
Published: 2022

14. Innate immune responses to Listeria in vivo

Author: Sylvain Levallois, Olivier Disson, Claire Maudet, Marc Lecuit, Biologie des Infections - Biology of Infection, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Paris (UP), Centre National de Référence Listeria - National Reference Center Listeria (CNRL), Centre collaborateur de l'OMS Listeria / WHO Collaborating Centre Listeria (CC-OMS / WHO-CC), Institut Pasteur [Paris]-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Service des Maladies infectieuses et tropicales [CHU Necker], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), Research in the Biology of Infection Unit is supported financially by Institut Pasteur, Inserm, ANR and ERC, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Cité (UPCité), Institut Pasteur [Paris] (IP)-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité)
Subjects: Microbiology (medical), [SDV]Life Sciences [q-bio], Placenta, Biology, medicine.disease_cause, Microbiology, 03 medical and health sciences, Listeria monocytogenes, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Pregnancy, In vivo, medicine, Humans, Listeriosis, Pathogen, 030304 developmental biology, 0303 health sciences, Innate immune system, 030306 microbiology, medicine.disease, biology.organism_classification, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, Immunity, Innate, 3. Good health, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, Infectious Diseases, Blood-Brain Barrier, Bacteremia, Host-Pathogen Interactions, Immunology, Listeria, Female, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract: International audience; Listeria monocytogenes (Lm) is a foodborne bacterial pathogen that causes listeriosis, a severe infection that manifests as bacteremia and meningo-encephalitis mostly in immunocompromised individuals, and maternal-fetal infection. A critical pathogenic determinant of Lm relies on its ability to actively cross the intestinal barrier, disseminate systemically and cross the blood-brain and placental barriers. Here we illustrate how Lm both evades innate immunity, favoring its dissemination in host tissues, and triggers innate immune defenses that participate to its control.
Published: 2021

15. Microbiota-induced active translocation of peptidoglycan across the intestinal barrier dictates its within-host dissemination

Author: Richard Wheeler, Paulo A. D. Bastos, Olivier Disson, Aline Rifflet, Julia Spielbauer, Marc Lecuit, and Ivo Gomperts Boneca
Abstract: Peptidoglycan, the major structural polymer forming the cell wall of bacteria, is an important mediator of physiological and behavioral effects in mammalian hosts. These effects are frequently linked to its translocation from the intestinal lumen to host tissues. However, the modality and regulation of this translocation across the gut barrier has not been precisely addressed. In this study, we characterized the absorption of peptidoglycan across the intestine and its systemic dissemination. We report that peptidoglycan has a distinct tropism for host organs when absorbed via the gut, most notably by favoring access to the brain. We demonstrate that intestinal translocation of peptidoglycan occurs through a microbiota-induced active process. This process is regulated by the parasympathetic pathway via the muscarinic acetylcholine receptors. Together, this study reveals fundamental parameters concerning the uptake of a major microbiota molecular signal from the steady-state gut.
Published: 2022

16. Bacterial inhibition of Fas-mediated killing promotes neuroinvasion and persistence

Author: Claire Maudet, Marouane Kheloufi, Sylvain Levallois, Julien Gaillard, Lei Huang, Charlotte Gaultier, Yu-Huan Tsai, Olivier Disson, Marc Lecuit, Biologie des Infections - Biology of Infection, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Centre National de Référence Listeria - National Reference Center Listeria (CNRL), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre collaborateur de l'OMS Listeria / WHO Collaborating Centre Listeria (CC-OMS / WHO-CC), Institut Pasteur [Paris] (IP)-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Service des Maladies infectieuses et tropicales [CHU Necker], CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Work in the M.L. laboratory is funded by the Institut Pasteur, Inserm, ERC, ANR, DIM1HEALTH, Labex IBEID (ANR-10-LABX-62-IBEID) and the Fondation Le Roch-Les Mousquetaires. C.M. and M.K. were recipients of the Roux-Cantarini fellowship of the Institut Pasteur. L.H., C.G. and J.G. were supported by the Université de Paris, Y.-H.T. by the Pasteur–Paris University (PPU) International PhD Program under the European Union’s Horizon 2020 research and innovation program, Marie Sklodowska-Curie grant agreement no 665807, and S.L. by FRM (ECO201906009119) and ‘Ecole Doctorale FIRE-Programme Bettencourt’., ANR-10-LABX-0062,IBEID,Integrative Biology of Emerging Infectious Diseases(2010), European Project: 665807,H2020,H2020-MSCA-COFUND-2014,PASTEURDOC(2015), DIAKITE, andrée, Integrative Biology of Emerging Infectious Diseases - - IBEID2010 - ANR-10-LABX-0062 - LABX - VALID, and Institut Pasteur International Docotal Program - PASTEURDOC - - H20202015-10-01 - 2020-10-01 - 665807 - VALID
Subjects: [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, Multidisciplinary, Virulence, [SDV]Life Sciences [q-bio], CD8-Positive T-Lymphocytes, Listeria monocytogenes, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, Monocytes, [SDV] Life Sciences [q-bio], Disease Models, Animal, Mice, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, Bacterial Proteins, Central Nervous System Diseases, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, [SDV.MHEP.MI] Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Animals, Listeriosis, [SDV.MP.BAC] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, [SDV.MP] Life Sciences [q-bio]/Microbiology and Parasitology, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract: International audience; Infections of the central nervous system are among the most serious infections1,2, but the mechanisms by which pathogens access the brain remain poorly understood. The model microorganism Listeria monocytogenes (Lm) is a major foodborne pathogen that causes neurolisteriosis, one of the deadliest infections of the central nervous system3,4. Although immunosuppression is a well-established host risk factor for neurolisteriosis3,5, little is known about the bacterial factors that underlie the neuroinvasion of Lm. Here we develop a clinically relevant experimental model of neurolisteriosis, using hypervirulent neuroinvasive strains6 inoculated in a humanized mouse model of infection7, and we show that the bacterial surface protein InlB protects infected monocytes from Fas-mediated cell death by CD8+ T cells in a manner that depends on c-Met, PI3 kinase and FLIP. This blockade of specific anti-Lm cellular immune killing lengthens the lifespan of infected monocytes, and thereby favours the transfer of Lm from infected monocytes to the brain. The intracellular niche that is created by InlB-mediated cell-autonomous immune resistance also promotes Lm faecal shedding, which accounts for the selection of InlB as a core virulence gene of Lm. We have uncovered a specific mechanism by which a bacterial pathogen confers an increased lifespan to the cells it infects by rendering them resistant to cell-mediated immunity. This promotes the persistence of Lm within the host, its dissemination to the central nervous system and its transmission.
Published: 2022

17. Listeria-associated lymphadenitis: a series of 11 consecutive cases and review of the literature

Author: Mathieu Blot, Olivier Disson, Alexandre Leclercq, Alexandra Moura, Hélène Bracq-Dieye, Pierre Thouvenot, Guillaume Valès, Barbara Burroni, Audrey Lupo, Marc Lecuit, Caroline Charlier, Centre National de Référence Listeria - National Reference Center Listeria (CNRL), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre collaborateur de l'OMS Listeria / WHO Collaborating Centre Listeria (CC-OMS / WHO-CC), Institut Pasteur [Paris] (IP)-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Service des Maladies infectieuses et tropicales [CHU Necker], CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Biologie des Infections - Biology of Infection, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), UFR Médecine [Santé] - Université Paris Cité (UFR Médecine UPCité), Université Paris Cité (UPCité), This work was funded by Institut Pasteur, Institut national de la santé et de la recherche médicale (INSERM), and Santé Publique France., We thank David Hardy (Experimental Neuropathology Unit, Institut Pasteur Paris) for section preparations. We thank Dr. Marie-Albane Bensussan (University Hospital, Amiens), Drs. Stéphane Bland and Helene Petitprez (Annecy-Genevois Hospital), Karine Aubry (University Hospital, Limoges), Dr. Burroni Barbara (Cochin University Hospital, Paris), Dr. Jean Puyhardy (HIA Legouest Hospital, Metz), and Dr. Barrans Alain (Bassin de Thau Hospital, Sete)., DIAKITE, andrée, and Université Paris Cité - UFR Médecine [Santé] (UPCité UFR Médecine)
Subjects: adenitis, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, Brief Report, [SDV]Life Sciences [q-bio], Listeria monocytogenes, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, [SDV] Life Sciences [q-bio], AcademicSubjects/MED00290, Infectious Diseases, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, Oncology, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, [SDV.MHEP.MI] Life Sciences [q-bio]/Human health and pathology/Infectious diseases, cancer, [SDV.MP.BAC] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, [SDV.MP] Life Sciences [q-bio]/Microbiology and Parasitology, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract: We studied 11 cases of culture-proven Listeria-associated lymphadenitis reported to the French National Reference Center for Listeria from 1994 to 2019 and 8 additional published cases. Listeria-associated lymphadenitis is rare, but it is associated with a mortality as high as for invasive listeriosis, and it is frequently diagnosed with concomitant neoplasia., We studied 11 cases of Listeria-associated lymphadenitis reported to the French Reference Center for Listeria, and 8 published cases. Listeria-associated lymphadenitis is rare but associated with a mortality as high as for invasive listeriosis, and frequently diagnosed with concomitant neoplasia.
Published: 2022

18. Live Imaging Reveals Listeria Hijacking of E-Cadherin Recycling as It Crosses the Intestinal Barrier

Author: Cindy Fevre, Marc Lecuit, Minhee Kim, Olivier Disson, Morgane Lavina, Biologie des Infections - Biology of Infection, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service des Maladies infectieuses et tropicales [CHU Necker], CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut Universitaire de France (IUF), Ministère de l'Education nationale, de l’Enseignement supérieur et de la Recherche (M.E.N.E.S.R.), Minhee Kim received a long-term postdoctoral fellowship from the European Molecular Biology Organization (EMBO), ALTF 1192-2017. Institut Pasteur, Inserm, LabEx IBEID, the European Research Council (ERC) Invadis and ANR Organolist provided financial support., ANR-10-LABX-0062,IBEID,Integrative Biology of Emerging Infectious Diseases(2010), ANR-15-CE15-0007,OrganoList,Interactions entre Listeria monocytogenes et la barrière intestinale(2015), European Project: 681829,ERC-CoG-2015,INVADIS(2016), and Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM)
Subjects: 0301 basic medicine, E-cadherin recycling, Listeria, [SDV]Life Sciences [q-bio], Vacuole, Biology, Endocytosis, medicine.disease_cause, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, 0302 clinical medicine, Bacterial Proteins, Listeria monocytogenes, Live cell imaging, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, medicine, Humans, Listeriosis, Internalin, intestine, organoids, Goblet cell, goblet cell, live imaging, Cadherins, Intestinal epithelium, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, 3. Good health, Cell biology, 030104 developmental biology, medicine.anatomical_structure, Transcytosis, Rab11, epithelial translocation, General Agricultural and Biological Sciences, 030217 neurology & neurosurgery, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract: International audience; Listeria monocytogenes is a foodborne bacterial pathogen that causes human listeriosis, a severe systemic infection [1]. Its translocation across the intestinal epithelium is mediated by the interaction of internalin (InlA), a Listeria surface protein, with its host species-specific receptor E-cadherin (Ecad) [2-5]. It occurs through goblet cells, on which Ecad is luminally accessible [6], via an unknown mechanism. In the absence of cell lines recapitulating this phenotype in vitro, we developed an ex vivo experimental system, based on the intraluminal microinjection of Listeria in untreated, pharmacologically-treated and genetically modified intestinal organoids. Using both live light sheet microscopy and confocal imaging, we show that Listeria translocates through goblet cells within a membrane vacuole in an InlA-and microtubule-dependent manner. As Ecad undergoes constant apical-basal recycling [7, 8], we hypothesized that Lm may transit through goblet cells by hijacking Ecad recycling pathway. Indeed, Listeria is stuck at goblet cell apex when Ecad endocytosis is blocked, and remains trapped intracellularly at the basolateral pole of goblet cells when Rab11-dependent Ecad recycling is compromised. Together, these results show that Listeria, upon docking onto its luminally accessible receptor Ecad, hijacks its recycling pathway to be transferred by transcytosis across goblet cells. Live imaging of host-pathogen interactions in organoids is a promising approach to dissect their underlying cell and molecular biology.
Published: 2021

19. Making Sense of the Biodiversity and Virulence of Listeria monocytogenes

Author: Olivier Disson, Alexandra Moura, Marc Lecuit, Biologie des Infections - Biology of Infection, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre National de Référence Listeria - National Reference Center Listeria (CNRL), Centre collaborateur de l'OMS Listeria / WHO Collaborating Centre Listeria (CC-OMS / WHO-CC), Institut Pasteur [Paris]-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Service des Maladies infectieuses et tropicales [CHU Necker], CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Research in the Biology of Infection Unit is supported financially by Institut Pasteur, Inserm, ANR and ERC. Marc Lecuit is a senior member of Institut Universitaire de France., ANR-10-LABX-0062,IBEID,Integrative Biology of Emerging Infectious Diseases(2010), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pasteur [Paris] (IP)-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), DIAKITE, andrée, and Integrative Biology of Emerging Infectious Diseases - - IBEID2010 - ANR-10-LABX-0062 - LABX - VALID
Subjects: Microbiology (medical), [SDV]Life Sciences [q-bio], Biodiversity, Virulence, Genomics, adaptation, Biology, medicine.disease_cause, Microbiology, 03 medical and health sciences, Listeria monocytogenes, listeriosis, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Virology, medicine, Animals, Humans, 030304 developmental biology, biodiversity, 0303 health sciences, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, 030306 microbiology, Intracellular parasite, Meningoencephalitis, medicine.disease, biology.organism_classification, Adaptation, Physiological, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, 3. Good health, [SDV] Life Sciences [q-bio], virulence, Infectious Diseases, [SDV.MHEP.MI] Life Sciences [q-bio]/Human health and pathology/Infectious diseases, [SDV.MP.BAC] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, Adaptation, Bacteria, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract: Listeria monocytogenes is a foodborne pathogen responsible for listeriosis, an infection that can manifest in humans as bacteremia, meningoencephalitis in immunocompromised patients and the elderly, and fetal-placental infection in pregnant women. Reference strains from this facultative intracellular bacterium have been instrumental in the investigation of basic mechanisms in microbiology, immunology, and cell biology. The integration of bacterial population genomics with environmental, epidemiological, and clinical data allowed the uncovering of new factors involved in the virulence of L. monocytogenes and its adaptation to different environments. This review illustrates how these investigations have led to a better understanding of the bacterium’s virulence and the driving forces that shaped it.
Published: 2021
Full Text: View/download PDF

20. Bacterial inhibition of CD8+T-cells mediated cell death promotes neuroinvasion and within-host persistence

Author: Lei Huang, Claire Maudet, Charlotte Gaultier, Marc Lecuit, Sylvain Levallois, Yu-Huan Tsai, Julien Gaillard, Marouane Kheloufi, Olivier Disson, Biologie des Infections - Biology of Infection, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Cité (UPCité), Centre National de Référence Listeria - National Reference Center Listeria (CNRL), Centre collaborateur de l'OMS Listeria / WHO Collaborating Centre Listeria (CC-OMS / WHO-CC), Institut Pasteur [Paris] (IP)-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Service des Maladies infectieuses et tropicales [CHU Necker], CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Work in ML laboratory is funded by Institut Pasteur, Inserm, ERC, ANR and Labex IBEID (ANR-10-LABX-62-IBEID). CM was a recipient of the Roux-Cantarini fellowship of Institut Pasteur. LH, CG and JG were supported by Université Paris Descartes, YHT by the Pasteur -Paris University (PPU) International PhD Program, under the European Union's Horizon 2020 research and innovation program, Marie Sklodowska-Curie grant agreement No 665807, and SL by FRM (ECO201906009119) and 'Ecole Doctorale FIRE–Programme Bettencourt'., ANR-10-LABX-0062,IBEID,Integrative Biology of Emerging Infectious Diseases(2010), European Project: 665807,H2020,H2020-MSCA-COFUND-2014,PASTEURDOC(2015), Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Paris (UP), Institut Pasteur [Paris]-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), DIAKITE, andrée, Integrative Biology of Emerging Infectious Diseases - - IBEID2010 - ANR-10-LABX-0062 - LABX - VALID, and Institut Pasteur International Docotal Program - PASTEURDOC - - H20202015-10-01 - 2020-10-01 - 665807 - VALID
Subjects: 0303 health sciences, Programmed cell death, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, 030306 microbiology, [SDV]Life Sciences [q-bio], Virulence, Biology, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, 3. Good health, Microbiology, [SDV] Life Sciences [q-bio], 03 medical and health sciences, Immune system, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Immunity, Humanized mouse, [SDV.MHEP.MI] Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Cytotoxic T cell, [SDV.MP.BAC] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, Pathogen, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, CD8, 030304 developmental biology
Abstract: Central nervous system infections are amongst the most severe1,2, yet the mechanisms by which pathogens access the brain remain poorly understood. The model microorganismListeria monocytogenes (Lm)is a major foodborne pathogen that causes neurolisteriosis, one of the deadliest central nervous system infections3,4. While immunosuppression is a well-established host risk factor for neurolisteriosis3,5, little is known regarding the bacterial factors underlyingLmneuroinvasion. We have developed a clinically-relevant experimental model of neurolisteriosis, using hypervirulent neuroinvasive strains6inoculated in a humanized mouse model of infection7, and we show that the bacterial protein InlB protects infected monocytes from CD8+T-cells Fas-mediated cell death, in a c-Met/PI3-kinase/FLIP-dependent manner. This blockade of anti-Lmspecific cellular immune response lengthens infected monocytes lifespan, favoringLmtransfer from infected monocytes to the brain. The intracellular niche created by InlB-mediated cell-autonomous immunosuppression also promotesLmfecal shedding, accounting for its selection as aLmcore virulence gene. Here, we have uncovered an unanticipated specific mechanism by which a bacterial pathogen confers to the cells it infects an increased lifespan by rendering them resistant to cell-mediated immunity. This promotesLmwithin-host persistence and dissemination to the central nervous system, and transmission.
Published: 2020

21. Maternal-neonatal listeriosis

Author: Marc Lecuit, Caroline Charlier, Olivier Disson, Biologie des Infections - Biology of Infection, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre National de Référence Listeria - National Reference Center Listeria (CNRL), Centre collaborateur de l'OMS Listeria / WHO Collaborating Centre Listeria (CC-OMS / WHO-CC), Institut Pasteur [Paris] (IP)-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Service des Maladies infectieuses et tropicales [CHU Necker], CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), This work was supported by the Institut Pasteur, Santé Publique France., DIAKITE, andrée, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), and Institut Pasteur [Paris]-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO)
Subjects: Microbiology (medical), placenta, [SDV]Life Sciences [q-bio], Immunology, macromolecular substances, Infectious and parasitic diseases, RC109-216, Biology, medicine.disease_cause, Microbiology, Infant, Newborn, Diseases, 03 medical and health sciences, Mice, Listeria monocytogenes, listeriosis, Risk Factors, newborn, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Placenta, medicine, Animals, Humans, Pregnancy Complications, Infectious, 030304 developmental biology, 0303 health sciences, Fetus, Pregnancy, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, 030306 microbiology, Infant, Newborn, medicine.disease, Infectious Disease Transmission, Vertical, infection, 3. Good health, Special Focus on Maternal-Fetal Infections, [SDV] Life Sciences [q-bio], fetus, Infectious Diseases, medicine.anatomical_structure, [SDV.MHEP.MI] Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Parasitology, Female, pregnancy, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, Neonatal Listeriosis
Abstract: International audience; Listeriosis is a rare and severe foodborne infection caused by Listeria monocytogenes. It manifests as septicemia, neurolisteriosis, and maternal-fetal infection. In pregnancy, it may cause maternal fever, premature delivery, fetal loss, neonatal systemic and central nervous system infections. Maternal listeriosis is mostly reported during the 2nd and 3rd trimester of pregnancy, as sporadic cases or in the context of outbreaks. Strains belonging to clonal complexes 1, 4 and 6, referred to as hypervirulent, are the most associated to maternal-neonatal infections. Here we review the clinical, pathophysiological, and microbiological features of maternal-neonatal listeriosis.
Published: 2020

22. Outbreak of Listeriosis in South Africa Associated with Processed Meat

Author: Vivien Essel, A.M. Shonhiwa, Kerrigan McCarthy, Tim Doyle, Nomsa P. Tau, Deon Mahoney, Alexandre Leclercq, Genevie Ntshoe, Olivier Disson, Mushal Allam, Robert W. Stewart, Adriano Duse, Mylène M. Maury, Teena Thomas, Hlengiwe M Ngomane, Linda Erasmus, Marc Lecuit, Arshad Ismail, Mathieu Tourdjman, Anthony M. Smith, Pierre Thouvenot, Juno Thomas, Bolele Disenyeng, Ntsieni Ramalwa, N. Govender, Lucille Blumberg, Nelesh P. Govender, Phuti Sekwadi, Shannon L. Smouse, Nicola Page, National Institute for Communicable Diseases [Johannesburg] (NICD), University of the Witwatersrand [Johannesburg] (WITS), Santé publique France - French National Public Health Agency [Saint-Maurice, France], Biologie des Infections - Biology of Infection, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre National de Référence Listeria - National Reference Center Listeria (CNRL), Centre collaborateur de l'OMS Listeria / WHO Collaborating Centre Listeria (CC-OMS / WHO-CC), Institut Pasteur [Paris]-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), Université de Paris (UP), Service des Maladies infectieuses et tropicales [CHU Necker], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pasteur [Paris] (IP)-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), and Université Paris Cité (UPCité)
Subjects: Adult, Male, Adolescent, [SDV]Life Sciences [q-bio], HIV Infections, 030204 cardiovascular system & hematology, Article, Disease Outbreaks, Foodborne Diseases, South Africa, Young Adult, 03 medical and health sciences, 0302 clinical medicine, Pregnancy, Environmental health, Humans, Medicine, Listeriosis, Processed meat, 030212 general & internal medicine, Pregnancy Complications, Infectious, Sex Distribution, Aged, Whole Genome Sequencing, business.industry, Infant, Newborn, Outbreak, General Medicine, Middle Aged, Listeria monocytogenes, Bacterial Typing Techniques, 3. Good health, Meat Products, Product Recalls and Withdrawals, Case-Control Studies, Food borne, HIV-1, Female, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, business, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract: International audience; BackgroundAn outbreak of listeriosis was identified in South Africa in 2017. The source was unknown.MethodsWe conducted epidemiologic, trace-back, and environmental investigations and used whole-genome sequencing to type Listeria monocytogenes isolates. A case was defined as laboratory-confirmed L. monocytogenes infection during the period from June 11, 2017, to April 7, 2018.ResultsA total of 937 cases were identified, of which 465 (50%) were associated with pregnancy; 406 of the pregnancy-associated cases (87%) occurred in neonates. Of the 937 cases, 229 (24%) occurred in patients 15 to 49 years of age (excluding those who were pregnant). Among the patients in whom human immunodeficiency virus (HIV) status was known, 38% of those with pregnancy-associated cases (77 of 204) and 46% of the remaining patients (97 of 211) were infected with HIV. Among 728 patients with a known outcome, 193 (27%) died. Clinical isolates from 609 patients were sequenced, and 567 (93%) were identified as sequence type 6 (ST6). In a case–control analysis, patients with ST6 infections were more likely to have eaten polony (a ready-to-eat processed meat) than those with non-ST6 infections (odds ratio, 8.55; 95% confidence interval, 1.66 to 43.35). Polony and environmental samples also yielded ST6 isolates, which, together with the isolates from the patients, belonged to the same core-genome multilocus sequence typing cluster with no more than 4 allelic differences; these findings showed that polony produced at a single facility was the outbreak source. A recall of ready-to-eat processed meat products from this facility was associated with a rapid decline in the incidence of L. monocytogenes ST6 infections.ConclusionsThis investigation showed that in a middle-income country with a high prevalence of HIV infection, L. monocytogenes caused disproportionate illness among pregnant girls and women and HIV-infected persons. Whole-genome sequencing facilitated the detection of the outbreak and guided the trace-back investigations that led to the identification of the source.
Published: 2020

23. Live Imaging Reveals Listeria Hijacking of E-Cadherin Recycling as It Crosses the Intestinal Barrier

Author: Morgane Lavina, Cindy Fevre, Marc Lecuit, Olivier Disson, and Minhee Kim
Subjects: Goblet cell, medicine.anatomical_structure, Listeria monocytogenes, Transcytosis, Live cell imaging, Chemistry, medicine, Internalin, Vacuole, medicine.disease_cause, Endocytosis, Intestinal epithelium, Cell biology
Abstract: Listeria monocytogenes is a foodborne bacterial pathogen that causes listeriosis, a severe systemic infection. Its translocation across the intestinal epithelium is mediated by the interaction of internalin (InlA), a Listeria surface protein, with its host species-specific receptor E-cadherin (Ecad). It occurs through goblet cells, on which Ecad is luminally accessible, via an unknown mechanism. In the absence of cell lines recapitulating this phenotype in vitro, we developed an ex vivo experimental system, based on the intraluminal microinjection of Listeria in untreated, pharmacologically-treated and genetically modified intestinal organoids. Using both live light sheet microscopy and confocal imaging, we show that Listeria translocates through goblet cells within a vacuole in an InlA- and microtubule-dependent manner. As Ecad undergoes constant apical-basal recycling, we hypothesized that Lm may transit through goblet cells by hijacking Ecad recycling pathway. Indeed, Listeria is stuck at goblet cell apex when Ecad endocytosis is blocked, and remains trapped intracellularly at the basolateral pole of goblet cells when Rab11-dependent Ecad recycling is compromised. Together, these results show that Listeria, upon docking onto its luminally accessible receptor Ecad, hijacks its recycling pathway to be transferred by transcytosis across goblet cells. Live imaging of host-pathogen interactions in organoids is a promising approach to dissect their underlying cell and molecular biology.
Published: 2020

24. Author Correction: Hypervirulent Listeria monocytogenes clones’ adaptation to mammalian gut accounts for their association with dairy products

Author: Morgane Lavina, Mylène M. Maury, Pierre Thouvenot, Olivier Disson, Guillaume Vales, Alexandre Leclercq, Marc Lecuit, Sylvain Brisse, Hélène Bracq-Dieye, and Lei Huang
Subjects: Food Handling, Science, General Physics and Astronomy, Food Contamination, Biology, medicine.disease_cause, General Biochemistry, Genetics and Molecular Biology, Microbial ecology, Foodborne Diseases, 03 medical and health sciences, Listeria monocytogenes, Bacterial genetics, Drug Resistance, Bacterial, medicine, Animals, Humans, lcsh:Science, Author Correction, Ecosystem, 030304 developmental biology, Genetics, 0303 health sciences, Multidisciplinary, Virulence, 030306 microbiology, General Chemistry, Adaptation, Physiological, Clone Cells, Intestines, Meat Products, Biofilms, Anti-Infective Agents, Local, lcsh:Q, Dairy Products, Adaptation, Pathogens, Benzalkonium Compounds
Abstract: Listeria monocytogenes (Lm) is a major human and animal foodborne pathogen. Here we show that hypervirulent Lm clones, particularly CC1, are strongly associated with dairy products, whereas hypovirulent clones, CC9 and CC121, are associated with meat products. Clone adaptation to distinct ecological niches and/or different food products contamination routes may account for this uneven distribution. Indeed, hypervirulent clones colonize better the intestinal lumen and invade more intestinal tissues than hypovirulent ones, reflecting their adaption to host environment. Conversely, hypovirulent clones are adapted to food processing environments, with a higher prevalence of stress resistance and benzalkonium chloride tolerance genes and a higher survival and biofilm formation capacity in presence of sub-lethal benzalkonium chloride concentrations. Lm virulence heterogeneity therefore reflects the diversity of the ecological niches in which it evolves. These results also have important public health implications and may help in reducing food contamination and improving food consumption recommendations to at-risk populations.
Published: 2019

25. IFITM proteins inhibit placental syncytiotrophoblast formation and promote fetal demise

Author: Thierry Fournier, Caroline Manet, Kenzo-Hugo Hillion, Thérèse Couderc, Emeline Perthame, Julian Buchrieser, Françoise Porrot, Séverine A. Degrelle, Marc Lecuit, Olivier Schwartz, Daniel A. Donahue, Quentin Nevers, Anne Dupressoir, Sylvie Souquere, Olivier Disson, Thierry Heidmann, Marlene V. Arroyo, Katinka Ruigrok, Xavier Montagutelli, Virus et Immunité - Virus and immunity, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Physiopathologie et pharmacotoxicologie placentaire humaine : Microbiote pré & post natal (3PHM - UMR-S 1139), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Inovarion [Paris], Biologie des Infections - Biology of Infection, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Génétique fonctionnelle de la Souris, Hub Bioinformatique et Biostatistique - Bioinformatics and Biostatistics HUB, Howard Hughes Medical Institute [New York] (HHMI), Howard Hughes Medical Institute (HHMI)-New York University School of Medicine, NYU System (NYU)-NYU System (NYU)-Rockefeller University [New York]-Columbia University Irving Medical Center (CUIMC), Analyse moléculaire, modélisation et imagerie de la maladie cancéreuse (AMMICa), Université Paris-Sud - Paris 11 (UP11)-Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Virologie Structurale - Structural Virology, Rétrovirus endogènes et éléments rétroïdes des eucaryotes supérieurs (UMR 9196), Université Paris-Sud - Paris 11 (UP11)-Institut Gustave Roussy (IGR)-Centre National de la Recherche Scientifique (CNRS), Université Paris Descartes - Paris 5 (UPD5), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Service des Maladies infectieuses et tropicales [CHU Necker], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Vaccine Research Institute (VRI), Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Work in the laboratory of O.S. is funded by Institut Pasteur, ANRS, Sidaction, the Vaccine Research Institute (ANR-10-LABX-77), Labex IBEID (ANR-10-LABX-62-IBEID), 'TIMTAMDEN' ANR-14-CE14-0029, 'CHIKV-Viro-Immuno' ANR-14-CE14-0015-01, CNRS and the Gilead HIV cure program. Work in the laboratory of M.L. is funded by Institut Pasteur, INSERM, ERC, Labex IBEID (ANR-10-LABX-62-IBEID), Institut Convergence, and Université Paris Descartes. C.M. was supported by a fellowship from grant no. ANR-10-LABX-62-IBEID. M.V.A. was supported by NSF GRFP grant no. 1644869., We thank members of the Virus and Immunity Unit for discussions and help, M. Maaran Rajah for critical reading of the manuscript. We thank patients who participated in the study. We also thank members of Embryology and Core Breeding teams (DTPS-C2RA-Central Animal Facility platform) for technical support with strain revivification, M. Cohen-Tannoudji for hosting mouse experiments. We thank the Cellular and Molecular Imaging facility of the Faculty of Pharmacy of Paris (UMS3612 CNRS/US25 INSERM), and the UtechS Photonic BioImaging (Imagopole)., ANR-10-LABX-0077,VRI,Initiative for the creation of a Vaccine Research Institute(2010), ANR-10-LABX-0062,IBEID,Integrative Biology of Emerging Infectious Diseases(2010), ANR-14-CE14-0029,TIMTAMDEN,Rôle des récepteurs TIM et TAM dans l'infection des cellules cibles par le virus de la dengue(2014), ANR-14-CE14-0015,CHIKV-Viro-Immuno,Multiplication et Relation avec l'hôte du virus Chikungunya(2014), Virus et Immunité - Virus and immunity (CNRS-UMR3569), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Vaccine Research Institute [Créteil, France] (VRI), Virus et Immunité, Centre National de la Recherche Scientifique (CNRS)-Institut Pasteur [Paris], Howard Hughes Medical Institute [New York], New York University School of Medicine, NYU System (NYU)-NYU System (NYU)-Columbia University Irving Medical Center (CUIMC)-Rockefeller University [New York], Virologie Structurale, Université Paris Descartes - Paris 5 (UPD5)-CHU Necker - Enfants Malades [AP-HP]-Institut des Maladies Génétiques Imagine [Paris], Institut des Maladies Génétiques Imagine [Paris], ANR-10-LABX-0077/10-LABX-0077,VRI,Initiative for the creation of a Vaccine Research Institute(2010), ANR-10-LABX-62-IBEID,IBEID,Laboratoire d'Excellence 'Integrative Biology of Emerging Infectious Diseases'(2010), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Descartes - Paris 5 (UPD5), Centre National de la Recherche Scientifique (CNRS)-Institut Gustave Roussy (IGR)-Université Paris-Sud - Paris 11 (UP11), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP)
Subjects: 0301 basic medicine, Fetal Resorption, [SDV]Life Sciences [q-bio], Endogeny, Pregnancy Proteins, Biology, Cell Fusion, Mice, 03 medical and health sciences, 0302 clinical medicine, Syncytiotrophoblast, Multinucleate, Pregnancy, Interferon, medicine, Animals, Humans, Fetal Death, Multidisciplinary, Cell fusion, Intracellular Signaling Peptides and Proteins, Gene Products, env, RNA-Binding Proteins, Trophoblast, Antigens, Differentiation, Transmembrane protein, Trophoblasts, 3. Good health, Cell biology, Poly I-C, 030104 developmental biology, medicine.anatomical_structure, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, Interferon Type I, [SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology, [SDV.IMM]Life Sciences [q-bio]/Immunology, Female, Apoptosis Regulatory Proteins, 030217 neurology & neurosurgery, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, medicine.drug
Abstract: Comment in Protecting fetal development. [Science. 2019]; International audience; Elevated levels of type I interferon (IFN) during pregnancy are associated with intrauterine growth retardation, preterm birth, and fetal demise through mechanisms that are not well understood. A critical step of placental development is the fusion of trophoblast cells into a multinucleated syncytiotrophoblast (ST) layer. Fusion is mediated by syncytins, proteins deriving from ancestral endogenous retroviral envelopes. Using cultures of human trophoblasts or mouse cells, we show that IFN-induced transmembrane proteins (IFITMs), a family of restriction factors blocking the entry step of many viruses, impair ST formation and inhibit syncytin-mediated fusion. Moreover, the IFN inducer polyinosinic:polycytidylic acid promotes fetal resorption and placental abnormalities in wild-type but not in Ifitm-deleted mice. Thus, excessive levels of IFITMs may mediate the pregnancy complications observed during congenital infections and other IFN-induced pathologies.
Published: 2019

26. Atypical Hemolytic Listeria innocua Isolates Are Virulent, albeit Less than Listeria monocytogenes

Author: Alexandra Moura, Alexandre Leclercq, Morgane Lavina, Olivier Disson, Athmanya K. Eshwar, Marc Lecuit, Maria Fredriksson-Ahomaa, Pierre Thouvenot, Lei Huang, Roger Stephan, Centre National de Référence Listeria - Biologie des Infections (CNRL), Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre collaborateur de l'OMS Listeria - Biologie des Infections (CCOMS), Biologie des Infections - Biology of Infection, Université Paris Diderot, Sorbonne Paris Cité, Paris, France, Université Paris Diderot - Paris 7 (UPD7), University of Helsinki, Institute for Food Safety and Hygiene, University of Zürich [Zürich] (UZH), Service des Maladies infectieuses et tropicales [CHU Necker], Université Paris Descartes - Paris 5 (UPD5)-CHU Necker - Enfants Malades [AP-HP]-Institut des Maladies Génétiques Imagine [Paris], Université Paris Descartes - Paris 5 (UPD5), CHU Necker - Enfants Malades [AP-HP], Institut des Maladies Génétiques Imagine [Paris], Centre National de Référence Listeria - National Reference Center Listeria (CNRL), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre collaborateur de l'OMS Listeria / WHO Collaborating Centre Listeria (CC-OMS / WHO-CC), Institut Pasteur [Paris] (IP)-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Helsingin yliopisto = Helsingfors universitet = University of Helsinki, Universität Zürich [Zürich] = University of Zurich (UZH), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Institut Pasteur [Paris]-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), University of Zurich, Freitag, Nancy E, and Lecuit, Marc
Subjects: inlA, L innocua, [SDV]Life Sciences [q-bio], 2405 Parasitology, LIPI, MESH: Virulence, medicine.disease_cause, MESH: Genome, Bacterial, MESH: Listeria monocytogenes, MESH: Bird Diseases, Feces, listeriosis, MESH: Listeria, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, MESH: Ducks, MESH: Genomic Islands, MESH: Animals, Galliformes, MESH: Phylogeny, MESH: Bacterial Proteins, Phylogeny, 2. Zero hunger, 0303 health sciences, biology, Strain (chemistry), 2404 Microbiology, MESH: Feces, MESH: Galliformes, 3. Good health, Infectious Diseases, medicine.anatomical_structure, Ducks, MESH: Whole Genome Sequencing, Genomic Islands, Listeria, Immunology, Virulence, 610 Medicine & health, Spleen, Microbiology, 03 medical and health sciences, Listeria monocytogenes, Bacterial Proteins, medicine, Animals, Humans, Internalin, Serotyping, Gene, 10082 Institute of Food Safety and Hygiene, 030304 developmental biology, 2403 Immunology, MESH: Humans, Whole Genome Sequencing, 030306 microbiology, Bird Diseases, MESH: Serotyping, 2725 Infectious Diseases, biology.organism_classification, Pathogenicity island, Molecular Pathogenesis, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, virulence, L. innocua, MESH: Listeriosis, 570 Life sciences, Parasitology, Genome, Bacterial, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract: International audience; Listeria innocua is considered a nonpathogenic Listeria species. Natural atypical hemolytic L. innocua isolates have been reported but have not been characterized in detail. Here, we report the genomic and functional characterization of representative isolates from the two known natural hemolytic L. innocua clades. Whole-genome sequencing confirmed the presence of Listeria pathogenicity islands (LIPI) characteristic of Listeria monocytogenes species. Functional assays showed that LIPI-1 and inlA genes are transcribed, and the corresponding gene products are expressed and functional. Using in vitro and in vivo assays, we show that atypical hemolytic L. innocua is virulent, can actively cross the intestinal epithelium, and spreads systemi-cally to the liver and spleen, albeit to a lesser degree than the reference L. monocy-togenes EGDe strain. Although human exposure to hemolytic L. innocua is likely rare, these findings are important for food safety and public health. The presence of viru-lence traits in some L. innocua clades supports the existence of a common virulent ancestor of L. monocytogenes and L. innocua.
Published: 2019

27. Listeria monocytogenes-associated endovascular infections: A study of 71 consecutive cases

Author: Guillaume Vales, Grégory Jouvion, Caroline Charlier, Gabrielle Coulpier, Olivier Disson, Marc Lecuit, Benoit Pilmis, Alexandre Leclercq, Pierre Thouvenot, Mylène M. Maury, Michka Shoai-Tehrani, Hélène Bracq-Dieye, Olivier Robineau, Laboratoire des Listeria, Centre National de Référence des Listeria, et Centre collaborateur de l’OMS pour la listériose d’origine alimentaire (CNR - CCOMS), Institut Pasteur [Paris], Service des Maladies infectieuses et tropicales [CHU Necker], CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Centre collaborateur de l'OMS Listeria / WHO Collaborating Centre Listeria (CC-OMS / WHO-CC), Institut Pasteur [Paris]-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Centre National de Référence Listeria - National Reference Center Listeria (CNRL), Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre Hospitalier de Tourcoing, Biologie des Infections - Biology of Infection, Neuropathologie expérimentale - Experimental neuropathology, Institut Pasteur [Paris]-Université Paris Descartes - Paris 5 (UPD5), Université Paris Descartes - Paris 5 (UPD5), This study received financial support from Institut Pasteur, Inserm and Santé Publique France., We thank Dr. Isabelle Serre (Gui Chauliac University Hospital, Montpellier, France), Dr. Valérie Hervieu (Edouard Herriot University Hospital, Lyon, France), Dr. Beatrice Luciani-Laillou (Périgueux, France) and Dr. Luc Marcellin (Hautepierre University Hospital, Strasbourg, France), David Hardy and Magali Tichit (Experimental Neuropathology Unit, Institut Pasteur, Paris) for their contribution to histopathology studies, as well as Giulia Nigro (Molecular Microbial Pathologenesis Unit, Institut Pasteur, Paris)., Institut Pasteur [Paris] (IP), Institut Pasteur [Paris] (IP)-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pasteur [Paris] (IP)-Université Paris Descartes - Paris 5 (UPD5), and DIAKITE, andrée
Subjects: 0301 basic medicine, Male, medicine.medical_treatment, [SDV]Life Sciences [q-bio], Prosthesis, medicine.disease_cause, Intracardiac injection, 0302 clinical medicine, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Risk Factors, Medicine, Listeriosis, 030212 general & internal medicine, Hospital Mortality, Aged, 80 and over, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, Endocarditis, Middle Aged, 3. Good health, [SDV] Life Sciences [q-bio], Infectious Diseases, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, Heart Valve Prosthesis, Epidemiological Monitoring, [SDV.MHEP.MI] Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Female, France, Microbiology (medical), medicine.medical_specialty, 030106 microbiology, 03 medical and health sciences, Aneurysm, Listeria monocytogenes, Humans, [SDV.MP] Life Sciences [q-bio]/Microbiology and Parasitology, Aged, Retrospective Studies, business.industry, Retrospective cohort study, Endocarditis, Bacterial, medicine.disease, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, Surgery, Heart failure, Concomitant, [SDV.MP.BAC] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, business, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract: International audience; Background: Listeria monocytogenes-associated endovascular infections are not well characterized. Methods: Retrospective study of 71 culture-proven cases reported to the French National Reference Center for Listeria from 1993 to 2018. Results: Seventy-one cases were identified: 42 with vascular aneurysms/prosthetic infections, 27 with endocarditis, 2 with both. Fifty-eight were men (82%); median age was 75 years [46-92]; 93% reported co-morbidities (66/71), including 50% with immunosuppressive conditions. Vascular infections consisted of infected aneurysms (68%) or prosthetic graft infections (32%); vascular rupture was reported in 25/42 (60%). Tissue samples grew L. monocytogenes in 98% (43/44) and blood cultures in 64% (27/42). Endo-carditis cases involved prosthetic or native valves or intracardiac devices in respectively 62% (18/29), 28% (8/29) and 10% (3/29). Infected valves were aortic (62%, 16/26), mitral (31%, 8/26) or both (8%, 2/26); 38% patients required surgery; 45% displayed heart failure; 17% had concomitant neurolisteriosis. In-hospital mortality in vascular infections was 12% (5/42) and 41% (12/29) for Lm-associated endocarditis. Conclusions: Endovascular listeriosis is a rare but severe infection. It manifests as vascular infections and endocarditis, mostly in older patients with vascular or cardiac valve prosthetic devices and co-morbidities. Mortality in Lm-associated endocarditis is twice higher than with other pathogens, requiring prompt recognition and treatment.
Published: 2019

28. Peyer’s patch myeloid cells infection by Listeria signals through gp38 + stromal cells and locks intestinal villus invasion

Author: James P. Di Santo, Grégory Jouvion, Sophie Dulauroy, Olivier Disson, Gérard Eberl, Nicolas Serafini, Grégoire Gessain, Marc Lecuit, Jean-Marie Jacob, Pierre Thouvenot, Lucie Peduto, Cindy Fevre, Camille Blériot, Biologie des Infections - Biology of Infection, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Stroma, inflammation et réparation tissulaire - Stroma, Inflammation and Tissue Repair, Immunité Innée - Innate Immunity, Microenvironnement et Immunité - Microenvironment and Immunity, Histopathologie humaine et Modèles animaux, Institut Pasteur [Paris] (IP), Université Paris Descartes - Paris 5 (UPD5), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), This work was financed by Institut Pasteur, Institut National de la Santé et de la Recherche Médicale, Institut Carnot Pasteur Microbes et Santé, LabEx IBEID, the European Research Council grant Invadis, and the Agence Nationale de Recherche Organolist., We thank the members of the Biology of Infection Unit for their support. We thank Hélène Bierne for her implication in the initial phase of the project, Elena Tomasello and Eric Vivier for helpful discussions, Stéphane Dallongeville for image analysis, Sascha Cording, Morgane Lavina for technical help, and Hana Kammoun for critical reading. We thank Edith Gouin and Pascale Cossart for anti-Lm antibodies, Tracy Putoczki for Il11ra1−/− mice, Richard Flavell for Il22−/− mice, Bernhard Ryffel for IL23p19−/− mice, Laure Dumoutier, Jean-Christophe Renauld for anti–IL-22 antibody, and Gunnar C. Hansson for anti-MUC2C3 serum, ANR-15-CE15-0007,OrganoList,Interactions entre Listeria monocytogenes et la barrière intestinale(2015), ANR-10-LABX-0062,IBEID,Integrative Biology of Emerging Infectious Diseases(2010), European Project: 681829,ERC-CoG-2015,INVADIS(2016), Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur [Paris], Institut Pasteur [Paris], DIAKITE, andrée, Interactions entre Listeria monocytogenes et la barrière intestinale - - OrganoList2015 - ANR-15-CE15-0007 - AAPG2015 - VALID, Integrative Biology of Emerging Infectious Diseases - - IBEID2010 - ANR-10-LABX-0062 - LABX - VALID, and Microbial invasion and dissemination within the host, mechanisms and effects - INVADIS - 2016-11-01 - 2021-10-31 - 681829 - VALID
Subjects: 0301 basic medicine, [SDV]Life Sciences [q-bio], Interleukin 22, Mice, Peyer's Patches, 0302 clinical medicine, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Immunology and Allergy, Listeriosis, Myeloid Cells, Intestinal Mucosa, Research Articles, Mice, Knockout, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, Membrane Glycoproteins, digestive, oral, and skin physiology, Colitis, Intestinal epithelium, 3. Good health, Cell biology, [SDV] Life Sciences [q-bio], medicine.anatomical_structure, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, 030220 oncology & carcinogenesis, [SDV.MHEP.MI] Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Cytokines, [SDV.IMM]Life Sciences [q-bio]/Immunology, STAT3 Transcription Factor, Stromal cell, [SDV.IMM] Life Sciences [q-bio]/Immunology, Immunology, Biology, digestive system, Article, 03 medical and health sciences, medicine, Animals, [SDV.MP] Life Sciences [q-bio]/Microbiology and Parasitology, Immunity, Mucosal, Lamina propria, Innate immune system, Intestinal villus, Peyer's patch, Listeria monocytogenes, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, Immunity, Innate, Epithelium, 030104 developmental biology, [SDV.MP.BAC] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, Stromal Cells, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract: Listeria monocytogenes (Lm) crosses the intestinal villus barrier via goblet cells (GCs). Disson et al. show that Lm infection of Peyer’s patch myeloid cells signals to villus stromal cells, leading to a decrease of GCs expressing luminally accessible E-cadherin, thereby blocking villus infection while favoring colitis., The foodborne pathogen Listeria monocytogenes (Lm) crosses the intestinal villus epithelium via goblet cells (GCs) upon the interaction of Lm surface protein InlA with its receptor E-cadherin. Here, we show that Lm infection accelerates intestinal villus epithelium renewal while decreasing the number of GCs expressing luminally accessible E-cadherin, thereby locking Lm portal of entry. This novel innate immune response to an enteropathogen is triggered by the infection of Peyer’s patch CX3CR1+ cells and the ensuing production of IL-23. It requires STAT3 phosphorylation in epithelial cells in response to IL-22 and IL-11 expressed by lamina propria gp38+ stromal cells. Lm-induced IFN-γ signaling and STAT1 phosphorylation in epithelial cells is also critical for Lm-associated intestinal epithelium response. GC depletion also leads to a decrease in colon mucus barrier thickness, thereby increasing host susceptibility to colitis. This study unveils a novel innate immune response to an enteropathogen, which implicates gp38+ stromal cells and locks intestinal villus invasion, but favors colitis., Graphical Abstract
Published: 2018

29. Le rôle critique de la PI3-kinase dans la traversée des barrières de l’hôte parListeria monocytogenes

Author: Grégoire Gessain, Olivier Disson, and Marc Lecuit
Subjects: 0301 basic medicine, Permissiveness, Chemistry, Kinase, General Medicine, Phosphatidylinositol 3-Kinases, medicine.disease_cause, Blood–brain barrier, General Biochemistry, Genetics and Molecular Biology, Microbiology, 03 medical and health sciences, Enzyme activator, 030104 developmental biology, medicine.anatomical_structure, Listeria monocytogenes, Intestinal mucosa, Placenta, medicine
Published: 2016

30. Translocation and dissemination to target neurons of botulinum neurotoxin type B in the mouse intestinal wall

Author: Olivier Disson, Carolina Varela-Chavez, Jordi Molgó, Alain Vandewalle, Georges Michel Haustant, Chloé Connan, Christelle Mazuet, Marc Lecuit, and Michel R. Popoff
Subjects: 0301 basic medicine, Cell type, Immunology, Chromosomal translocation, Anatomy, Biology, Endocytosis, Microbiology, Intestinal epithelium, Synaptotagmin 1, Cell biology, 03 medical and health sciences, 030104 developmental biology, medicine.anatomical_structure, Cell surface receptor, Virology, Lymph circulation, medicine, Neuron
Abstract: Botulinum neurotoxins (BoNTs) are responsible for severe flaccid paralysis (botulism), which in most cases enter the organism via the digestive tract and then disseminate into the blood or lymph circulation to target autonomic and motor nerve endings. The passage way of BoNTs alone or in complex forms with associated nontoxic proteins through the epithelial barrier of the digestive tract still remains unclear. Here, we show using an in vivo model of mouse ligated intestinal loop that BoNT/B alone or the BoNT/B C-terminal domain of the heavy chain (HCcB), which interacts with cell surface receptors, translocates across the intestinal barrier. The BoNT/B or HCcB translocation through the intestinal barrier occurred via an endocytosis-dependent mechanism within 10-20 min, because Dynasore, a potent endocytosis inhibitor, significantly prevented BoNT/B as well as HCcB translocation. We also show that HCcB or BoNT/B specifically targets neuronal cells and neuronal extensions in the intestinal submucosa and musculosa expressing synaptotagmin, preferentially cholinergic neurons and to a lower extent other neuronal cell types, notably serotonergic neurons. Interestingly, rare intestinal epithelial cells accumulated HCcB suggesting that distinct cell types of the intestinal epithelium, still undefined, might mediate efficient translocation of BoNT/B.
Published: 2015

31. Spontaneous Loss of Virulence in Natural Populations of Listeria monocytogenes

Author: Mariela Scortti, Alexandra Moura, Lei Han, Guillaume Vales, Alexandre Leclercq, Olivier Disson, Marc Lecuit, Hélène Bracq-Dieye, Mylène M. Maury, Edith Gouin, José A. Vázquez-Boland, Viviane Chenal-Francisque, Centre collaborateur de l'OMS Listeria / WHO Collaborating Centre Listeria (CC-OMS / WHO-CC), Institut Pasteur [Paris] (IP)-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Centre National de Référence Listeria - National Reference Center Listeria (CNRL), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), University of Edinburgh, Biologie des Infections - Biology of Infection, Interactions Bactéries-Cellules (UIBC), Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Descartes - Paris 5 (UPD5), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Work in M.L.'s laboratory was supported by Institut Pasteur, Inserm, LabEx IBEID, the European Research Council, and Santé Publique France. Work in J.A.V.-B.'s laboratory was supported by the Wellcome Trust (program grant WT074020MA) and partially by core Roslin Institute funding from BBSRC (BB/J004227/1), We acknowledge Anne Morvan, Thomas Cantinelli, Nathalie Tessaud-Rita and Laetitia Bellon for their help in strain collection and isolation at the National Reference Centre for Listeria. We thank Pascale Cossart for providing antibodies against LLO and the Institut Pasteur P2M platform for genome sequencing., ANR-10-LABX-0062,IBEID,Integrative Biology of Emerging Infectious Diseases(2010), DIAKITE, andrée, Integrative Biology of Emerging Infectious Diseases - - IBEID2010 - ANR-10-LABX-0062 - LABX - VALID, Institut Pasteur [Paris]-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), Centre collaborateur de l'OMS Listeria - Biologie des Infections (CCOMS), Centre National de Référence Listeria - Biologie des Infections (CNRL), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur [Paris]-Institut National de la Recherche Agronomique (INRA), Institut des Maladies Génétiques Imagine [Paris], and ANR-10-LABX-62-IBEID,IBEID,Laboratoire d'Excellence 'Integrative Biology of Emerging Infectious Diseases'(2010)
Subjects: 0301 basic medicine, Erythrocytes, MESH: Selection, Genetic, Mutant, MESH: Heat-Shock Proteins, MESH: Virulence, medicine.disease_cause, MESH: Listeria monocytogenes, Severity of Illness Index, MESH: Recombinant Proteins, Hemolysin Proteins, Mice, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Listeriosis, MESH: Animals, Cloning, Molecular, MESH: Phylogeny, Pathogen, MESH: Bacterial Proteins, Heat-Shock Proteins, Phylogeny, Mice, Inbred BALB C, MESH: Gene Expression Regulation, Bacterial, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, MESH: Erythrocytes, Listeriolysin O, Biological Evolution, spontaneous mutations, MESH: Amino Acid Substitution, MESH: Hemolysis, Recombinant Proteins, Infectious Diseases, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, MESH: Hemolysin Proteins, [SDV.MHEP.MI] Life Sciences [q-bio]/Human health and pathology/Infectious diseases, MESH: Peptide Termination Factors, Peptide Termination Factors, Transposable element, MESH: Mutation, Bacterial Toxins, 030106 microbiology, Immunology, MESH: Mice, Inbred BALB C, Virulence, Molecular Genomics, MESH: Biological Evolution, Biology, Microbiology, Frameshift mutation, 03 medical and health sciences, Bacterial Proteins, Listeria monocytogenes, MESH: Severity of Illness Index, medicine, genomics, Animals, Humans, MESH: Cloning, Molecular, Selection, Genetic, [SDV.MP] Life Sciences [q-bio]/Microbiology and Parasitology, Gene, MESH: Mice, MESH: Humans, Gene Expression Regulation, Bacterial, biochemical phenomena, metabolism, and nutrition, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, virulence, Amino Acid Substitution, MESH: Bacterial Toxins, MESH: Listeriosis, Mutation, Parasitology, [SDV.MP.BAC] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, hemolysis, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract: The pathogenesis of Listeria monocytogenes depends on the ability of this bacterium to escape from the phagosome of the host cells via the action of the pore-forming toxin listeriolysin O (LLO). Expression of the LLO-encoding gene ( hly ) requires the transcriptional activator PrfA, and both hly and prfA genes are essential for L. monocytogenes virulence. Here, we used the hemolytic activity of LLO as a phenotypic marker to screen for spontaneous virulence-attenuating mutations in L. monocytogenes . Sixty nonhemolytic isolates were identified among a collection of 57,820 confirmed L. monocytogenes strains isolated from a variety of sources (0.1%). In most cases (56/60; 93.3%), the nonhemolytic phenotype resulted from nonsense, missense, or frameshift mutations in prfA . Five strains carried hly mutations leading to a single amino acid substitution (G299V) or a premature stop codon causing strong virulence attenuation in mice. In one strain, both hly and gshF (encoding a glutathione synthase required for full PrfA activity) were missing due to genomic rearrangements likely caused by a transposable element. The PrfA/LLO loss-of-function (PrfA − /LLO − ) mutants belonged to phylogenetically diverse clades of L. monocytogenes , and most were identified among nonclinical strains (57/60). Consistent with the rare occurrence of loss-of-virulence mutations, we show that prfA and hly are under purifying selection. Although occurring at a low frequency, PrfA − /LLO − mutational events in L. monocytogenes lead to niche restriction and open an evolutionary path for obligate saprophytism in this facultative intracellular pathogen.
Published: 2017

32. LISTERIA MONOCYTOGENES

Author: null Alexandre LECLERCQ, null Caroline CHARLIER-WOERTHER, null Olivier DISSON, null Christine JACQUET, null Paul MARTIN, null Jocelyne ROCOURT, and null Marc LECUIT
Abstract: Sur la base de caractères morphologiques (petit bacille à Grampositif), Listeria a été longtemps considérée comme une bactériecorynéforme. D’un point de vue taxonomique, Listeria appartient au règne des Bacteria, à l’embranchement des Firmicutes,à la classe des Bacilli, à l’ordre des Bacillales et à la familledes Listeriaceae. Dans les phylogrammes obtenus à partir desséquences de l’ADNr 16S, elle se positionne dans la branchedes Clostridium, Staphylococcus, Streptococcus, Lactobacilluset d’autres bacilles à Gram positif ayant un G+C% inférieur à50% ; celui des Listeria varie de 36 à 45% (1).
Published: 2019

33. Uncovering Listeria monocytogenes hypervirulence by harnessing its biodiversity

Author: Mylène M. Maury, Olivier Disson, Marc Lecuit, Sophie Roussel, Yu Huan Tsai, Alexis Criscuolo, Sylvain Brisse, Viviane Chenal-Francisque, Alexandre Leclercq, Eduardo P. C. Rocha, Caroline Charlier, Marie Touchon, Anne Brisabois, Charlotte Gaultier, DIAKITE, andrée, Integrative Biology of Emerging Infectious Diseases - - IBEID2010 - ANR-10-LABX-0062 - LABX - VALID, Subversive pro- and anti-inflammation trade-offs promote infection by Listeria monocytogenes - Infect-ERA/0001/2013 - - FCT::2014-09-01 - 2017-08-31 - 137216 - VALID, Cellule Pasteur, Université Paris Diderot - Paris 7 (UPD7)-PRES Sorbonne Paris Cité, Génomique évolutive des Microbes / Microbial Evolutionary Genomics, Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Biologie des Infections - Biology of Infection, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre collaborateur de l'OMS Listeria / WHO Collaborating Centre Listeria (CC-OMS / WHO-CC), Institut Pasteur [Paris] (IP)-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Université Paris Descartes - Paris 5 (UPD5), Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Centre National de Référence Listeria - National Reference Center Listeria (CNRL), Centre de Bioinformatique, Biostatistique et Biologie Intégrative (C3BI), Université Paris-Est (UPE), Laboratoire de sécurité des aliments de Maisons-Alfort (LSAl), Agence nationale de sécurité sanitaire de l'alimentation, de l'environnement et du travail (ANSES), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), This study was funded by the Institut Pasteur, INSERM, from the French government's Investissement d'Avenir program, Laboratoire d'Excellence 'Integrative Biology of Emerging Infectious Diseases' (grant ANR-10-LABX-62-IBEID), the European Research Council (ERC), ERANET Proantilis, the Programme Hospitalier de Recherche Clinique MONALISA and the Programme de Recherche Translationnelle (PTR) ANSES–Institut Pasteur. Listeriosis surveillance in France is funded by the Institut de Veille Sanitaire (InVS) and the Institut Pasteur., We thank C. Soto Alvarez, G. Pontdeme, T. Cantinelli and L. Diancourt for their contributions to MLST data production and analysis, and S. Roche for providing low-virulence strains for genome sequencing. We also thank D. Mornico (Center of Bioinformatics, Biostatistics and Integrative Biology of the Institut Pasteur) for his help with the submission of genome reads and assemblies., ANR-10-LABX-0062,IBEID,Integrative Biology of Emerging Infectious Diseases(2010), European Project: 137216,FCT::,Infect-ERA/2013,Infect-ERA/0001/2013(2014), Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pasteur [Paris]-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP)
Subjects: Central Nervous System, 0301 basic medicine, 030106 microbiology, Virulence, Genomics, Biology, medicine.disease_cause, Article, Microbiology, Mice, 03 medical and health sciences, Listeria monocytogenes, Phylogenetics, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Gene cluster, Genetics, medicine, Animals, Humans, Listeriosis, [SDV.MP] Life Sciences [q-bio]/Microbiology and Parasitology, Phylogeny, 2. Zero hunger, Comparative genomics, Biodiversity, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, 030104 developmental biology, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, Humanized mouse, [SDV.MHEP.MI] Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Microbial genetics, [SDV.MP.BAC] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, Genome-Wide Association Study
Abstract: Corrigendum: Uncovering Listeria monocytogenes hypervirulence by harnessing its biodiversity. [Nat Genet. 2017]Erratum: Uncovering Listeria monocytogenes hypervirulence by harnessing its biodiversity. [Nat Genet. 2017]Comment in Biodiversity and hypervirulence of Listeria monocytogenes. [Nat Genet. 2016] Bacterial GWAS: not just gilding the lily. [Nat Rev Microbiol. 2016]; International audience; Microbial pathogenesis studies are typically performed with reference strains, thereby overlooking within-species heterogeneity in microbial virulence. Here we integrated human epidemiological and clinical data with bacterial population genomics to harness the biodiversity of the model foodborne pathogen Listeria monocytogenes and decipher the basis of its neural and placental tropisms. Taking advantage of the clonal structure of this bacterial species, we identify clones epidemiologically associated either with food or with human central nervous system (CNS) or maternal-neonatal (MN) listeriosis. The latter clones are also most prevalent in patients without immunosuppressive comorbidities. Strikingly, CNS- and MN-associated clones are hypervirulent in a humanized mouse model of listeriosis. By integrating epidemiological data and comparative genomics, we have uncovered multiple new putative virulence factors and demonstrate experimentally the contribution of the first gene cluster mediating L. monocytogenes neural and placental tropisms. This study illustrates the exceptional power in harnessing microbial biodiversity to identify clinically relevant microbial virulence attributes
Published: 2016

34. PI3-kinase activation is critical for host barrier permissiveness to Listeria monocytogenes

Author: Olivier Disson, Caroline Charlier, Solène Grayo, Yu Huan Tsai, Marc Lecuit, Pascale Cossart, Grégoire Gessain, Laetitia Travier, Matteo Bonazzi, Cellule Pasteur, Université Paris Diderot - Paris 7 (UPD7)-PRES Sorbonne Paris Cité, Biologie des Infections - Biology of Infection, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Diderot - Paris 7 (UPD7), Interactions Bactéries-Cellules (UIBC), Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Imagine - Institut des maladies génétiques (IMAGINE - U1163), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre collaborateur de l'OMS Listeria / WHO Collaborating Centre Listeria (CC-OMS / WHO-CC), Institut Pasteur [Paris] (IP)-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Centre National de Référence Listeria - National Reference Center Listeria (CNRL), Université Paris Descartes - Paris 5 (UPD5), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut Pasteur, Inserm, FRM, Ville de Paris, fondation AXA, fondation BNP Paribas, LabEx IBEID, ERC, European Project: 261157,EC:FP7:ERC,ERC-2010-StG_20091118,MICROTRANS(2010), Disson, Olivier, Microbial translocation across host barriers - MICROTRANS - - EC:FP7:ERC2010-11-01 - 2016-10-31 - 261157 - VALID, Lecuit, Marc, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pasteur [Paris]-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur [Paris]-Institut National de la Recherche Agronomique (INRA), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre collaborateur de l'OMS Listeria - Biologie des Infections (CCOMS), and Centre National de Référence Listeria - Biologie des Infections (CNRL)
Subjects: Permissiveness, Immunology, Plasma protein binding, [SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], [SDV.BC.IC] Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB], medicine.disease_cause, Article, Enzyme activator, Phosphatidylinositol 3-Kinases, 03 medical and health sciences, 0302 clinical medicine, Listeria monocytogenes, Intestinal mucosa, Pregnancy, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, [SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB], medicine, [SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], Immunology and Allergy, Animals, Humans, Listeriosis, Subcellular Processes, 030304 developmental biology, 0303 health sciences, Phosphoinositide 3-kinase, biology, Cadherin, SDV:MP:BAC, Cell Biology, bacterial infections and mycoses, Virology, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, Cell biology, SDV:BC:IC, 030220 oncology & carcinogenesis, Host-Pathogen Interactions, biology.protein, [SDV.MHEP.MI] Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Female, Organisation et fonctions cellulaires, Signal transduction, [SDV.MP.BAC] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, SDV:MHEP:MI
Abstract: Gessain et al. explore how Listeria monocytogenes facilitates disseminated infection through host epithelial barriers using two of its surface proteins, InlA and InlB. By combining in vitro and in vivo approaches using intestinal and placental mouse and human tissues, they find a differential requirement for InlA and InlB in tissue invasiveness, with a critical role for PI3K activation., Invasion of nonphagocytic cells, a critical property of Listeria monocytogenes (Lm) that enables it to cross host barriers, is mediated by the interaction of two bacterial surface proteins, InlA and InlB, with their respective receptors E-cadherin and c-Met. Although InlA–E-cadherin interaction is necessary and sufficient for Lm crossing of the intestinal barrier, both InlA and InlB are required for Lm crossing of the placental barrier. The mechanisms underlying these differences are unknown. Phosphoinositide 3-kinase (PI3-K) is involved in both InlA- and InlB-dependent pathways. Indeed, InlA-dependent entry requires PI3-K activity but does not activate it, whereas InlB–c-Met interaction activates PI3-K. We show that Lm intestinal target cells exhibit a constitutive PI3-K activity, rendering InlB dispensable for InlA-dependent Lm intestinal barrier crossing. In contrast, the placental barrier does not exhibit constitutive PI3-K activity, making InlB necessary for InlA-dependent Lm placental invasion. Here, we provide the molecular explanation for the respective contributions of InlA and InlB to Lm host barrier invasion, and reveal the critical role of InlB in rendering cells permissive to InlA-mediated invasion. This study shows that PI3-K activity is critical to host barrier permissiveness to microbes, and that pathogens exploit both similarities and differences of host barriers to disseminate.
Published: 2015

35. Liver-Resident Macrophage Necroptosis Orchestrates Type 1 Microbicidal Inflammation and Type-2-Mediated Tissue Repair during Bacterial Infection

Author: Grégory Jouvion, Camille Blériot, Olivier Disson, Théo Dupuis, Marc Lecuit, Gérard Eberl, Biologie des Infections - Biology of Infection, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Histopathologie humaine et Modèles animaux, Institut Pasteur [Paris], Développement des Tissus Lymphoïdes, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Université Paris Descartes - Paris 5 (UPD5), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Service des Maladies infectieuses et tropicales [CHU Necker], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), This work was financed by Institut Pasteur, Institut National de la Santé et de la Recherche Médicale, Institut Carnot, Fondation pour la Recherche Médicale, Ville de Paris, Fondation BNP Paribas, LabEx IBEID, the European Research Council, and Listress EU program., We thank the members of the Biology of Infection Unit, and in particular Y.H. Tsai. We thank G. Milon and S. Berrè for helpful discussions and critical reading of the manuscript. We thank H. Bierne for her contribution in the initial phase of the project and P. Cossart for providing the Lm Δhly mutant. We thank T. Walzer at ENS Lyon for Ccr2−/− mice, Ph. Bousso and F. Montalvao for MaFIA-GFP mice and helpful discussions, M. Leite de Moraes for Il4−/− mice, B. Ryffel for Il1rl1−/− mice, V. Dixit for Rip3−/− mice, T. Taniguchi for Irf3−/− mice, R. Menard for Flk1-gfp mice, and M. Albert and N. Yatim for Casp1−/− and Ifnar−/− mice and helpful discussions. We thank S. Novault of the PFC at Institut Pasteur and N. Sérafini for their help in the FACS experiments., ANR-10-LABX-0062,IBEID,Integrative Biology of Emerging Infectious Diseases(2010), European Project: 116472,FCT::,ERA-PTG/2010,ERA-PTG/0003/2010(2011), Université Paris Descartes - Paris 5 (UPD5)-CHU Necker - Enfants Malades [AP-HP]-Institut des Maladies Génétiques Imagine [Paris], Institut des Maladies Génétiques Imagine [Paris], ANR-10-LABX-62-IBEID,IBEID,Laboratoire d'Excellence 'Integrative Biology of Emerging Infectious Diseases'(2010), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pasteur [Paris] (IP), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité)
Subjects: MESH: Inflammation, Necrosis, Cellular differentiation, [SDV]Life Sciences [q-bio], Complement Pathway, Alternative, MESH: Listeria monocytogenes, MESH: Monocytes, Monocytes, Mice, 0302 clinical medicine, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Macrophage, Immunology and Allergy, Homeostasis, Listeriosis, MESH: Animals, MESH: Phagocytosis, Cells, Cultured, 0303 health sciences, Kupffer cell, Cell Differentiation, medicine.anatomical_structure, Infectious Diseases, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, Liver, MESH: Homeostasis, [SDV.IMM]Life Sciences [q-bio]/Immunology, medicine.symptom, MESH: Cells, Cultured, MESH: Cell Differentiation, MESH: Interleukins, MESH: Interleukin-33, Kupffer Cells, Necroptosis, Immunology, Inflammation, Mice, Inbred Strains, Biology, MESH: Mice, Inbred Strains, 03 medical and health sciences, Immune system, Phagocytosis, medicine, Animals, MESH: Mice, 030304 developmental biology, MESH: Necrosis, Wound Healing, Monocyte, Interleukins, MESH: Interleukin-4, Interleukin-33, Listeria monocytogenes, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, MESH: Wound Healing, MESH: Kupffer Cells, MESH: Listeriosis, Interleukin-4, MESH: Complement Pathway, Alternative, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, 030215 immunology, MESH: Liver
Abstract: International audience; Kupffer cells, the phagocytes of fetal origin that line the liver sinusoids, are key contributors of host defense against enteroinvasive bacteria. Here, we found that infection by Listeria monocytogenes induced the early necroptotic death of Kupffer cells, which was followed by monocyte recruitment and an anti-bacterial type 1 inflammatory response. Kupffer cell death also triggered a type 2 response that involved the hepatocyte-derived alarmin interleukin-33 (IL-33) and basophil-derived interleukin-4 (IL-4). This led to the alternative activation of the monocyte-derived macrophages recruited to the liver, which thereby replaced ablated Kupffer cells and restored liver homeostasis. Kupffer cell death is therefore a key signal orchestrating type 1 microbicidal inflammation and type-2-mediated liver repair upon infection. This indicates that beyond the classical dichotomy of type 1 and type 2 responses, these responses can develop sequentially in the context of a bacterial infection and act interdependently, orchestrating liver immune responses and return to homeostasis, respectively.
Published: 2015

36. Role for Brm in Cell Growth Control

Author: Marjorie Coisy-Quivy, Jean-Christophe Dantonel, Olivier Disson, Jean-Marie Blanchard, Christian Muchardt, and Virginie Roure
Subjects: G2 Phase, Cancer Research, biology, Cell growth, Kinase, Cell Cycle, Cyclin A, Mitosis, 3T3 Cells, Cell Growth Processes, Fibroblasts, Cell cycle, Chromatin remodeling, Cell biology, Mice, Gene Expression Regulation, Oncology, Chromosome Segregation, biology.protein, Animals, Kinase activity, Cell Division, Transcription Factors, Cyclin, Anaphase
Abstract: Recently, we have shown implication of Brm, the catalytic subunit of the SWI/SNF chromatin remodeling complex, in repression of cyclin A expression in quiescent cells. Here, we have examined the fate of cells lacking Brm throughout the cycle. We find that despite elevated levels of cyclins A and E, these cells can respond to serum starvation, however, without reaching a canonical G0 phase as they continue to express high levels of c-Myc and have an abnormally large average size. The response to serum starvation can be correlated with increased levels of Rb proteins p130 and p107 as well as increased association of p27 with the cyclin-dependent kinases, possibly compensating for the higher levels of G1 cyclins by reducing their associated kinase activity. After serum stimulation, reentry into the cycle occurs normally, but the S phase is delayed and shorter. In addition, the M phase has an increased duration, and we observed frequent faulty chromosome segregation events in anaphase. Altogether, our data suggest that cells can partially overcome the absence of Brm by activating several compensatory mechanisms to control the cell cycle. However, they remain profoundly affected, unable to enter a canonical quiescent state, presenting a shorter S phase, and finally unable to perform correct chromosome segregation. (Cancer Res 2006; 66(10): 5069-76)
Published: 2006

37. In vivo RNA localization of I factor, a non-LTR retrotransposon, requires a cis-acting signal in ORF2 and ORF1 protein

Author: Maria del Carmen Seleme, Stéphanie Robin, Danielle Teninges, Olivier Disson, Alain Bucheton, and Christine Brun
Subjects: RNA localization, Retroelements, Retrotransposon, Biology, Regulatory Sequences, Ribonucleic Acid, Article, Transposition (music), Oogenesis, Genetics, medicine, Animals, Drosophila Proteins, RNA, Messenger, Ribonucleoprotein, Sequence Deletion, Base Sequence, RNA, RNA-Directed DNA Polymerase, Molecular biology, Cell biology, Complementation, medicine.anatomical_structure, Phenotype, Cytoplasm, Mutation, Oocytes, Drosophila, Female, Nucleus
Abstract: According to the current model of non-LTR retrotransposon (NLR) mobilization, co-expression of the RNA transposition intermediate, and the proteins it encodes (ORF1p and ORF2p), is a requisite for the formation of cytoplasmic ribonucleoprotein complexes which contain necessary elements to complete a retrotransposition cycle later in the nucleus. To understand these early processes of NLR mobilization, here we analyzed in vivo the protein and RNA expression patterns of the I factor, a model NLR in Drosophila. We show that ORF1p and I factor RNA, specifically produced during transposition, are co-expressed and tightly co-localize with a specific pattern (Loc+) exclusively in the cytoplasm of germ cells permissive for retrotransposition. Using an ORF2 mutated I factor, we show that ORF2p plays no role in the Loc+ patterning. With deletion derivatives of an I factor we define an RNA localization signal required to display the Loc+ pattern. Finally, by complementation experiments we show that ORF1p is necessary for the efficient localization of I factor RNA. Our data suggest that ORF1p is involved in proper folding and stabilization of I factor RNA for efficient targeting, through Loc+ patterning, to the nuclear neighborhood where downstream steps of the retrotransposition process occur.
Published: 2005

38. Erratum: Uncovering Listeria monocytogenes hypervirulence by harnessing its biodiversity

Author: Caroline Charlier, Alexis Criscuolo, Yu-Huan Tsai, Olivier Disson, Marie Touchon, Viviane Chenal-Francisque, Sophie Roussel, Eduardo P. C. Rocha, Alexandre Leclercq, Charlotte Gaultier, Mylène M. Maury, Sylvain Brisse, Anne Brisabois, and Marc Lecuit
Subjects: 0301 basic medicine, 03 medical and health sciences, 030104 developmental biology, Listeria monocytogenes, Genetics, medicine, Biodiversity, Biology, medicine.disease_cause, Microbiology
Abstract: Nat. Genet. 48, 308–313 (2016); published online 1 February 2016; corrected after print 6 March 2017 In the version of this article initially published, the titles of the x axes in Figure 5b and 5c should have been “Brain/blood CFU ratio” instead of “Blood/brain CFU ratio,” and the title of the z axis in Figure 2c should have been “% of isolates” instead of “Number of isolates.
Published: 2017

39. Erratum: Corrigendum: Uncovering Listeria monocytogenes hypervirulence by harnessing its biodiversity

Author: Anne Brisabois, Eduardo P. C. Rocha, Marie Touchon, Sophie Roussel, Viviane Chenal-Francisque, Yu-Huan Tsai, Caroline Charlier, Marc Lecuit, Alexandre Leclercq, Mylène M. Maury, Charlotte Gaultier, Olivier Disson, Sylvain Brisse, and Alexis Criscuolo
Subjects: 0301 basic medicine, 03 medical and health sciences, 030104 developmental biology, Listeria monocytogenes, Cns infections, Genetics, Biodiversity, medicine, Biology, medicine.disease_cause, Microbiology
Abstract: Nat. Genet. 48, 308–313 (2016); published online 1 February 2016; corrected after print 6 March 2017 In the version of this article initially published, in Figure 2b, in the panel called “CNS infections” the bar of CC3 should have been represented in red and the one of CC121 should have been represented in blue.
Published: 2017

40. Méningite néonatale à streptocoque du groupe B

Author: Isabelle Tardieux, Claire Poyart, Marc Lecuit, Abdelouhab Bouaboud, Olivier Disson, Patrick Trieu-Cuot, Asmaa Tazi, and Samuel Bellais
Subjects: 0303 health sciences, 03 medical and health sciences, 030306 microbiology, General Medicine, General Biochemistry, Genetics and Molecular Biology, 030304 developmental biology, 3. Good health
Abstract: Le streptocoque du groupe B (SGB, Streptococcus agalactiae ) est une bacterie capsulee a Gram positif commensale des voies digestives et vaginales retrouvee chez 20 a 30 % des adultes sains. Son interet en medecine humaine reside principalement dans le fait que cette bacterie est la premiere cause d’infections neonatales invasives (septicemies, meningites) et un pathogene d’importance croissante chez l’adulte, en particulier chez le sujet âge et les individus porteurs de pathologies sousjacentes [].
Published: 2011

41. In vitro and in vivo models to study human listeriosis: mind the gap

Author: Olivier Disson and Marc Lecuit
Subjects: media_common.quotation_subject, Immunology, Cell, Intracellular Space, Vacuole, Biology, medicine.disease_cause, Microbiology, Listeria monocytogenes, Bacterial Proteins, medicine, Animals, Humans, Listeriosis, Internalization, media_common, Intracellular parasite, Membrane Proteins, In vitro, Infectious Diseases, medicine.anatomical_structure, Cell culture, Host-Pathogen Interactions, Intracellular
Abstract: Listeria monocytogenes (Lm) is the etiological agent of listeriosis, one of the deadliest human foodborne infections. Lm is able to cross the intestinal, placental and blood–brain barriers, leading to septicemia, fetoplacental infection, meningitis and encephalitis. The intracellular life cycle of this facultative intracellular bacterium has been studied in detail in in vitro cell culture systems. Lm enters in non-phagocytic cells in an InlA–Ecad and/or InB-Met dependent manner. Lm then escapes from its internalization vacuole via the action of the pore forming toxin LLO and spreads from cell to cell in an ActA-dependent manner. In vivo studies in “humanized” mouse models and human epidemiological data have led to the deciphering of the mechanisms underlying Lm crossing of intestinal and placental barriers. As illustrated in this review, in vivo outcomes could not be deduced directly from in vitro observations, and led to revisit the intracellular fate of Lm during infection.
Published: 2013

42. Concepts and Mechanisms: Crossing Host Barriers

Author: Kelly S. Doran, Olivier Disson, Anirban Banerjee, Marc Lecuit, San Diego State University (SDSU), University of California [San Diego] (UC San Diego), University of California, Biologie des Infections - Biology of Infection, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Descartes - Paris 5 (UPD5), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Service des Maladies infectieuses et tropicales [CHU Necker], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), Work on the BBB and bacterial meningitis in K.S.D.’s laboratory is supported by funding from the National Institutes of Health/National Institute of Neurological Disorders and Stroke (grant No. RO1NS051247). Work in M.L’s laboratory is supported by Institut Pasteur, INSERM, ERC, FRM, Ville de Paris, Labex IBEID, Listress, and ICRES EU Programs and Fondation BNP-Paribas. The authors declare no competing financial interests., The authors thank their respective laboratory members for their help and support and apologize to researchers whose work has not been discussed in detail or reviewed here because of space constraints., ANR-10-LABX-0062,IBEID,Integrative Biology of Emerging Infectious Diseases(2010), ANR-10-PATH-0001,LISTRESS(2010), University of California (UC), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité)
Subjects: Immune defense, Placenta, [SDV]Life Sciences [q-bio], Biology, Bacterial translocation, Bacterial Adhesion, General Biochemistry, Genetics and Molecular Biology, Microbiology, 03 medical and health sciences, Phagocytosis, Intestinal mucosa, Pregnancy, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Animals, Humans, Barrier integrity, Parasites, Intestinal Mucosa, Skin, 030304 developmental biology, Inflammation, 0303 health sciences, Bacteria, 030306 microbiology, Host (biology), Cell biology, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, Blood-Brain Barrier, Bacterial Translocation, Host-Pathogen Interactions, Viruses, [SDV.IMM]Life Sciences [q-bio]/Immunology, Female, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, Perspectives
Abstract: International audience; The human body is bordered by the skin and mucosa, which are the cellular barriers that define the frontier between the internal milieu and the external nonsterile environment. Additional cellular barriers, such as the placental and the blood-brain barriers, define protected niches within the host. In addition to their physiological roles, these host barriers provide both physical and immune defense against microbial infection. Yet, many pathogens have evolved elaborated mechanisms to target this line of defense, resulting in a microbial invasion of cells constitutive of host barriers, disruption of barrier integrity, and systemic dissemination and invasion of deeper tissues. Here we review representative examples of microbial interactions with human barriers, including the intestinal, placental, and blood-brain barriers, and discuss how these microbes adhere to, invade, breach, or compromise these barriers.
Published: 2013

43. ActA promotes Listeria monocytogenes aggregation, intestinal colonization and carriage

Author: Jean-Marc Ghigo, Marc Lecuit, Viviane Chenal-Francisque, Edith Gouin, Olivier Disson, Alexandre Dufour, Stéphanie Guadagnini, Pascale Cossart, Laetitia Travier, Jean-Christophe Olivo-Marin, Biologie des Infections - Biology of Infection, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Microscopie ultrastructurale (plate-forme), Institut Pasteur [Paris], Interactions Bactéries-Cellules (UIBC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur [Paris]-Institut National de la Recherche Agronomique (INRA), Analyse d'Images Quantitative (AIQ), Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Centre collaborateur de l'OMS Listeria - Biologie des Infections (CCOMS), Génétique des Biofilms, Centre d'infectiologie Necker-Pasteur [CHU Necker], CHU Necker - Enfants Malades [AP-HP], This work received financial support of the Institut Pasteur (http://www.pasteur.fr/ip/easysite/pasteur/en), the Institut National de la Santé et de la Recherche Médicale (Inserm) (http://www.inserm.fr/), the Fondation pour la Recherche Médicale (FRM) (http://www.frm.org/), the European Research Council (ERC) (http://erc.europa.eu/), the Mairie de Paris (http://www.paris.fr/) and the BNP Paribas Foundation (http://www.bnpparibas.com/nous-connaitre/mecenat/fondation-bnp-paribas)., We thank Cindy Fèvre, Delphine Judith, Camille Blériot and Lilliana Radoshevich, Alexandre Leclercq and Marie-Christine Prevost for helpful discussions and critical reading of the manuscript. We thank Didier Cabanes, the students of the 2003–2004 Institut Pasteur Microbiology Course and Prof. O Dussurget for the EGDe ΔactA (BUG2167) and EGD ΔprfA (BUG2141) strains., Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur [Paris], Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre collaborateur de l'OMS Listeria / WHO Collaborating Centre Listeria (CC-OMS / WHO-CC), Institut Pasteur [Paris]-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut Pasteur [Paris], Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pasteur [Paris] (IP), Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Institut Pasteur [Paris] (IP)-Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Institut Pasteur [Paris] (IP)-CHU Necker - Enfants Malades [AP-HP], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)
Subjects: Bacterial Diseases, [SDV]Life Sciences [q-bio], Pathogenesis, medicine.disease_cause, Feces, Mice, fluids and secretions, Intestinal mucosa, Gastrointestinal tract, Listeriosis, Gastrointestinal Infections, Intestinal Mucosa, Biology (General), Pathogen, Cecum, 0303 health sciences, Microbial Growth and Development, Animal Models, Bacterial Pathogens, Host-Pathogen Interaction, Infectious Diseases, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, Host-Pathogen Interactions, embryonic structures, Medicine, Bacterial and Foodborne Illness, Intracellular, Research Article, Virulence Factors, Colon, QH301-705.5, Immunology, Virulence, Motility, Gastroenterology and Hepatology, macromolecular substances, Biology, Microbiology, Cell Line, 03 medical and health sciences, Model Organisms, Listeria monocytogenes, Bacterial Proteins, Virology, Genetics, medicine, Animals, Humans, Actin polymerization, Molecular Biology, Microbial Pathogens, 030304 developmental biology, FLOW BIOFILM FORMATION, ARP2/3 COMPLEX, SURFACE PROTEIN, VIRULENCE GENES, EGD-E, DISINFECTANT RESISTANCE, FECAL CARRIAGE, TAIL FORMATION, E-CADHERIN, MOTILITY, Intracellular pathogens, 030306 microbiology, Intracellular parasite, Biofilm, technology, industry, and agriculture, Membrane Proteins, Bacteriology, RC581-607, Actins, Disease Models, Animal, Bacterial biofilms, Biofilms, bacteria, Parasitology, Immunologic diseases. Allergy
Abstract: Listeria monocytogenes (Lm) is a ubiquitous bacterium able to survive and thrive within the environment and readily colonizes a wide range of substrates, often as a biofilm. It is also a facultative intracellular pathogen, which actively invades diverse hosts and induces listeriosis. So far, these two complementary facets of Lm biology have been studied independently. Here we demonstrate that the major Lm virulence determinant ActA, a PrfA-regulated gene product enabling actin polymerization and thereby promoting its intracellular motility and cell-to-cell spread, is critical for bacterial aggregation and biofilm formation. We show that ActA mediates Lm aggregation via direct ActA-ActA interactions and that the ActA C-terminal region, which is not involved in actin polymerization, is essential for aggregation in vitro. In mice permissive to orally-acquired listeriosis, ActA-mediated Lm aggregation is not observed in infected tissues but occurs in the gut lumen. Strikingly, ActA-dependent aggregating bacteria exhibit an increased ability to persist within the cecum and colon lumen of mice, and are shed in the feces three order of magnitude more efficiently and for twice as long than bacteria unable to aggregate. In conclusion, this study identifies a novel function for ActA and illustrates that in addition to contributing to its dissemination within the host, ActA plays a key role in Lm persistence within the host and in transmission from the host back to the environment., Author Summary Listeria monocytogenes (Lm) is a ubiquitous bacterium that survives and thrives within the environment, and a facultative intracellular pathogen that induces listeriosis. So far, these two complementary facets of Lm biology have been studied independently. Here we identify ActA, which is a major Lm virulence determinant mediating actin-based motility, as critical for bacterial aggregation and biofilm formation. ActA promotes Lm aggregation via direct ActA-ActA interaction and ActA C-terminal region, which is not involved in actin polymerization, is essential for aggregation. Whereas ActA-mediated Lm aggregation is not observed in infected tissues, it occurs in the gut lumen. Strikingly, ActA-dependent aggregating bacteria exhibit an increased ability to persist within the gut lumen, and are shed in the feces three order of magnitude more and for twice as long than bacteria unable to aggregate. This study identifies a novel function for ActA, which plays a key role in Lm persistence within the host and transmission.
Published: 2013

44. Targeting of the central nervous system by Listeria monocytogenes

Author: Marc Lecuit, Olivier Disson, DIAKITE, andrée, Microorganismes et Barrières de l'Hôte (Equipe avenir), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre National de Référence des Listeria-G5 Microorganismes et Barrières de l'Hôte (CNR-CCOMS), Institut Pasteur [Paris] (IP), Centre d'infectiologie Necker-Pasteur [CHU Necker], Institut Pasteur [Paris] (IP)-CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Université Paris Descartes - Paris 5 (UPD5), Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pasteur [Paris], CHU Necker - Enfants Malades [AP-HP], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut Pasteur [Paris]
Subjects: [SDV]Life Sciences [q-bio], Meningitis, Listeria, Review, medicine.disease_cause, MESH: Listeria monocytogenes, MESH: Blood-Brain Barrier, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, MESH: Animals, 0303 health sciences, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, Meningoencephalitis, Ruminants, 3. Good health, [SDV] Life Sciences [q-bio], Infectious Diseases, medicine.anatomical_structure, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, Blood-Brain Barrier, MESH: Ruminants, Host-Pathogen Interactions, [SDV.MHEP.MI] Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Meningitis, Microbiology (medical), Immunology, Central nervous system, Biology, Blood–brain barrier, Microbiology, 03 medical and health sciences, Listeria monocytogenes, In vivo, medicine, Animals, Humans, [SDV.MP] Life Sciences [q-bio]/Microbiology and Parasitology, 030304 developmental biology, MESH: Humans, 030306 microbiology, Intracellular parasite, MESH: Host-Pathogen Interactions, medicine.disease, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, In vitro, Disease Models, Animal, Parasitology, [SDV.MP.BAC] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, MESH: Disease Models, Animal, MESH: Meningitis, Listeria, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract: International audience; Among bacteria that reach the central nervous system (CNS), Listeria monocytogenes (Lm) is one of deadliest, in human and ruminant. This facultative intracellular bacterium has the particularity to induce meningitis, meningoencephalitis and rhombencephalitis. Mechanisms by which Lm accesses the CNS remain poorly understood, but two major routes of infection have been proposed, based on clinical, in vitro and in vivo observations. A retrograde neural route is likely to occur in ruminants upon crossing of the oral epithelium, and this probably accounts for the observation that Lm induces almost exclusively rhombencephalitis in these animals. In contrast, the hematogenous route is likely the most frequent in human, in whom bacteria circulating in the blood, either free or associated with leukocytes are thought to breach the blood-brain barrier. New animal models that faithfully reproduce the hallmarks of human neurolisterisosis will allow addressing the molecular mechanisms underlying Lm ability to induce CNS disease, and improve our understanding of the pathophysiology of this deadly infection.
Published: 2012

45. Transcytosis of Listeria monocytogenes across the intestinal barrier upon specific targeting of goblet cell accessible E-cadherin

Author: Pascale Cossart, Théodora Niault, Marc Lecuit, Olivier Disson, Georgios Nikitas, Chantal Deschamps, Microorganismes et Barrières de l'Hôte (Equipe avenir), Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Interactions Bactéries-Cellules (UIBC), Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre d'infectiologie Necker-Pasteur [CHU Necker], CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut Pasteur [Paris], Centre National de Référence des Listeria-G5 Microorganismes et Barrières de l'Hôte (CNR-CCOMS), Institut Pasteur [Paris], Georgios Nikitas received a Marie Curie Early Stage Research Training fellowship from the Intrapath program, EU FP6. We thank Institut Pasteur, Institut National de la Santé et de la Recherche Médicale, Fondation pour la Recherche Médicale, Ville de Paris, Fondation BNP Paribas, and the European Research Council for financial support., We thank the members of the Microbes and Host Barriers Group for their support and Matteo Bonazzi and the personnel of the Imagopole Facility for their help and support. We thank Gerard Eberl for helpful discussion and advice., European Project: 35418,INTRAPATH, Equipe avenir Microorganismes et Barrières de l'Hôte, Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur [Paris]-Institut National de la Recherche Agronomique (INRA), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pasteur [Paris] (IP)-CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), and Institut Pasteur [Paris] (IP)
Subjects: MESH: Transcytosis, INVASION, MESH: Listeria monocytogenes, CAMPYLOBACTER-JEJUNI, MESH: Cadherins, Mice, Intestinal mucosa, Immunology and Allergy, Listeriosis, MESH: Animals, Intestinal Mucosa, IN-VIVO, 0303 health sciences, MESH: Exocytosis, Tight junction, SURFACE PROTEIN, Cell Polarity, respiratory system, Cadherins, Intestinal epithelium, 3. Good health, Cell biology, TRANSLOCATION, medicine.anatomical_structure, Transcytosis, MESH: Intestinal Mucosa, Goblet Cells, NEISSERIA-GONORRHOEAE, MESH: Cell Polarity, EPITHELIAL TIGHT JUNCTION, MESH: Mice, Transgenic, Immunology, Mice, Transgenic, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Biology, digestive system, Exocytosis, Article, Microbiology, Adherens junction, 03 medical and health sciences, MESH: Mice, Inbred C57BL, medicine, Animals, Humans, ESCHERICHIA-COLI K1, MESH: Mice, 030304 developmental biology, Goblet cell, Mucous Membrane, MESH: Humans, 030306 microbiology, Cadherin, MESH: Mucous Membrane, Listeria monocytogenes, Epithelium, Mice, Inbred C57BL, MESH: Listeriosis, MESH: Biomarkers, CACO-2 CELLS, MESH: Goblet Cells, Biomarkers, RAT SMALL-INTESTINE
Abstract: Listeria monocytogenes targets accessible E-cadherin expressed on mucus-producing goblet cells to invade the intestinal tissue., Listeria monocytogenes (Lm) is a foodborne pathogen that crosses the intestinal barrier upon interaction between its surface protein InlA and its species-specific host receptor E-cadherin (Ecad). Ecad, the key constituent of adherens junctions, is typically situated below tight junctions and therefore considered inaccessible from the intestinal lumen. In this study, we investigated how Lm specifically targets its receptor on intestinal villi and crosses the intestinal epithelium to disseminate systemically. We demonstrate that Ecad is luminally accessible around mucus-expelling goblet cells (GCs), around extruding enterocytes at the tip and lateral sides of villi, and in villus epithelial folds. We show that upon preferential adherence to accessible Ecad on GCs, Lm is internalized, rapidly transcytosed across the intestinal epithelium, and released in the lamina propria by exocytosis from where it disseminates systemically. Together, these results show that Lm exploits intrinsic tissue heterogeneity to access its receptor and reveal transcytosis as a novel and unanticipated pathway that is hijacked by Lm to breach the intestinal epithelium and cause systemic infection.
Published: 2011

46. The surface protein HvgA mediates group B streptococcus hypervirulence and meningeal tropism in neonates

Author: Samuel Bellais, Huot Khun, Nicolas Dmytruk, Charlotte Mechler, Asmaa Tazi, Claire Poyart, Patrick Trieu-Cuot, Michel-Yves Mistou, Olivier Disson, Marc Lecuit, Shaynoor Dramsi, Abdelouhab Bouaboud, Isabelle Tardieux, Institut Cochin (IC UM3 (UMR 8104 / U1016)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre national de Référence des Streptocoques (CNR), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Microorganismes et Barrières de l'Hôte (Equipe avenir), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur [Paris], Biologie des Bactéries Pathogènes à Gram-positif, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Histotechnologie et Pathologie, Institut Pasteur [Paris], Hôpital Louis Mourier - AP-HP [Colombes], Université Paris Descartes - Paris 5 (UPD5), CHU Necker - Enfants Malades [AP-HP], Service des Maladies infectieuses et tropicales [CHU Necker], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), This work was supported by the Agence Nationale de la Recherche (ANR HyperVirGBS Project, ANR-08-MIE-015), Institut National de la Santé et de la Recherche Médicale, Institut Pasteur, Fondation pour la Recherche Médicale (FRM), Université Paris Descartes, the Institut de Veille Sanitaire, Programme Transversal de Recherche #190. S. Bellais was a recipient of a post-doctoral fellowship from the ANR-08-MIE-015 grant and O. Disson from FRM and Institut National de la Santé et de la Recherche Médicale., We are grateful to Alexandra Gruss for helpful discussion and critical reading of the manuscript. We thank Pierre-Olivier Couraud for providing HCMEC/D3 cells., ANR-08-MIEN-0015,HYPERVIRGBS,Rôle de la protéine Gbs2018C dans l'hypervirulence du clone ST-17 du Streptocoque du groupe B(2008), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Institut Pasteur [Paris] (IP), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP), Equipe avenir Microorganismes et Barrières de l'Hôte, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Hopital Louis Mourier - AP-HP [Colombes], and Université Paris Descartes - Paris 5 (UPD5)-CHU Necker - Enfants Malades [AP-HP]-Institut des Maladies Génétiques Imagine [Paris]
Subjects: Male, MESH: Adhesins, Bacterial, [SDV]Life Sciences [q-bio], medicine.disease_cause, Bacterial Adhesion, MESH: Blood-Brain Barrier, Mice, Meninges, MESH: Streptococcal Infections, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Immunology and Allergy, MESH: Animals, Intestinal Mucosa, MESH: Organ Specificity, 0303 health sciences, Streptococcus, MESH: Infant, Newborn, MESH: Infant, 3. Good health, Intestines, MESH: Meningitis, Bacterial, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, Blood-Brain Barrier, Organ Specificity, MESH: Intestinal Mucosa, Female, Meningitis, MESH: Intestines, MESH: Bacterial Translocation, MESH: Meninges, Immunology, Virulence, Context (language use), Biology, Meningitis, Bacterial, Streptococcus agalactiae, Microbiology, Neonatal meningitis, 03 medical and health sciences, Streptococcal Infections, medicine, Animals, Humans, MESH: Bacterial Adhesion, Adhesins, Bacterial, MESH: Mice, Tropism, 030304 developmental biology, MESH: Humans, 030306 microbiology, Infant, Newborn, Brief Definitive Report, Infant, medicine.disease, MESH: Streptococcus agalactiae, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, MESH: Male, Bacterial adhesin, Bacterial Translocation, MESH: HeLa Cells, MESH: Female, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, HeLa Cells
Abstract: Lethal meningitis triggered by the hypervirulent group B streptococcus clone ST-17 is mediated by a novel surface protein called HvgA., Streptococcus agalactiae (group B streptococcus; GBS) is a normal constituent of the intestinal microflora and the major cause of human neonatal meningitis. A single clone, GBS ST-17, is strongly associated with a deadly form of the infection called late-onset disease (LOD), which is characterized by meningitis in infants after the first week of life. The pathophysiology of LOD remains poorly understood, but our epidemiological and histopathological results point to an oral route of infection. Here, we identify a novel ST-17–specific surface-anchored protein that we call hypervirulent GBS adhesin (HvgA), and demonstrate that its expression is required for GBS hypervirulence. GBS strains that express HvgA adhered more efficiently to intestinal epithelial cells, choroid plexus epithelial cells, and microvascular endothelial cells that constitute the blood–brain barrier (BBB), than did strains that do not express HvgA. Heterologous expression of HvgA in nonadhesive bacteria conferred the ability to adhere to intestinal barrier and BBB-constituting cells. In orally inoculated mice, HvgA was required for intestinal colonization and translocation across the intestinal barrier and the BBB, leading to meningitis. In conclusion, HvgA is a critical virulence trait of GBS in the neonatal context and stands as a promising target for the development of novel diagnostic and antibacterial strategies.
Published: 2010

47. The Issue of Species Specificity of Bacterial Infection, How to Address it Experimentally

Author: Pascale Cossart, Olivier Disson, and Marc Lecuit
Subjects: biology, Listeria, biology.organism_classification, Pathogen, Virology, Microbiology
Published: 2010

48. Human Listeriosis Caused by Listeria ivanovii

Author: Olivier Disson, Alban Le Monnier, Magdalena K. Bielecka, Olivier Join-Lambert, Christelle Guillet, Marie-France Mamzer-Bruneel, Patrick Berche, Mariela Scortti, Marc Lecuit, Alexandre Leclercq, Frédéric Méchaï, Olivier Lortholary, José A. Vázquez-Boland, Université Paris Descartes - Paris 5 (UPD5), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut Pasteur [Paris], University of Edinburgh, Universidad Complutense de Madrid = Complutense University of Madrid [Madrid] (UCM), Institut National de la Santé et de la Recherche Médicale (INSERM), Universidad de León [León], M.L. received financial support from Assistance Publique–Hôpitaux de Paris, Université Paris Descartes, Institut Pasteur, Institut de Veille Sanitaire, and Institut National de la Santé et de la Recherche Médicale. J.V.-B. received Wellcome Trust program grant 074020., We thank Véronique Goulet for helpful discussions., and Institut Pasteur [Paris] (IP)
Subjects: Male, Epidemiology, [SDV]Life Sciences [q-bio], lcsh:Medicine, Human pathogen, MESH: Listeria, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, MESH: Immunocompromised Host, Listeriosis, MESH: Animals, bacteria, MESH: Bacteremia, 0303 health sciences, [SDV.MHEP.ME]Life Sciences [q-bio]/Human health and pathology/Emerging diseases, MESH: Middle Aged, biology, Goats, MESH: Paris, dispatch, Middle Aged, 3. Good health, Infectious Diseases, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, Listeria ivanovii, gastroenteritis, Microbiology (medical), Paris, Listeria, kidney transplantation, Opportunistic Infections, MESH: Goats, Microbiology, lcsh:Infectious and parasitic diseases, Immunocompromised Host, 03 medical and health sciences, medicine, Animals, Humans, lcsh:RC109-216, bacteremia, 030304 developmental biology, MESH: Humans, 030306 microbiology, lcsh:R, MESH: Opportunistic Infections, biology.organism_classification, medicine.disease, Virology, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, MESH: Gastroenteritis, MESH: Male, MESH: Listeriosis, Bacteremia, Bacteria, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract: International audience; Two species of Listeria are pathogenic; L. monocytogenes infects humans and animals, and L. ivanovii has been considered to infect ruminants only. We report L. ivanovii–associated gastroenteritis and bacteremia in a man. This isolate was indistinguishable from prototypic ruminant strains. L. ivanovii is thus an enteric opportunistic human pathogen.The genus Listeria contains 2 pathogenic species, L. monocytogenes and L. ivanovii (1). They both invade host cells, replicate in the cytosol after phagosomal escape, and spread from cell to cell by polymerizing actin. These mechanisms correlate with the presence in each species of genetic determinants called the inlAB internalization locus, the LIPI-1 intracellular survival pathogenicity island, and the hpt intracellular growth locus (2). However, each species appears to infect different hosts: L. monocytogenes infects humans and ruminants, whereas L. ivanovii is thought to infect ruminants only (2). L. ivanovii have been previously isolated, although rarely, from infected humans, indicating pathogenic potential for humans (Table). We report a case of L. ivanovii infection in a man with a kidney transplant. The ecology of L. ivanovii suggests that the rarity of human listeriosis due to this species reflects not only host tropism factors but also the rare occurrence of this species in the environment, compared with L. monocytogenes.
Published: 2010

49. Real-Time Observation of Listeria monocytogenes-Phagocyte Interactions in Living Zebrafish Larvae

Author: Philippe Herbomel, Pascale Cossart, Isabelle Bonne, Karima Kissa, Marc Lecuit, Jean-Pierre Levraud, Olivier Disson, Macrophages et Développement de l'Immunité, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Microorganismes et Barrières de l'Hôte (Equipe avenir), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur [Paris], Microscopie ultrastructurale (plate-forme), Institut Pasteur [Paris], Interactions Bactéries-Cellules (UIBC), Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Descartes - Paris 5 (UPD5), Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pasteur [Paris] (IP), Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), and DIAKITE, andrée
Subjects: Phagocyte, Neutrophils, [SDV]Life Sciences [q-bio], Human pathogen, MESH: Neutrophils, MESH: Heat-Shock Proteins, medicine.disease_cause, MESH: Phagocytes, MESH: Listeria monocytogenes, MESH: Cadherins, Hemolysin Proteins, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Macrophage, MESH: Animals, Zebrafish, MESH: Bacterial Proteins, Heat-Shock Proteins, Phagosome, Phagocytes, 0303 health sciences, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, Bacterial Infections, Cadherins, 3. Good health, [SDV] Life Sciences [q-bio], Infectious Diseases, medicine.anatomical_structure, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, MESH: Hemolysin Proteins, Larva, [SDV.MHEP.MI] Life Sciences [q-bio]/Human health and pathology/Infectious diseases, MESH: Membrane Proteins, animal structures, Virulence Factors, Bacterial Toxins, Immunology, Virulence, Biology, Microbiology, 03 medical and health sciences, Bacterial Proteins, Listeria monocytogenes, medicine, Animals, MESH: Zebrafish, [SDV.MP] Life Sciences [q-bio]/Microbiology and Parasitology, 030304 developmental biology, MESH: Virulence Factors, Innate immune system, 030306 microbiology, Macrophages, fungi, Membrane Proteins, MESH: Macrophages, biology.organism_classification, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, MESH: Bacterial Toxins, Parasitology, [SDV.MP.BAC] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, MESH: Larva, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract: The zebrafish,Danio rerio, has become a popular vertebrate model for the study of infections, mainly because of its excellent optical accessibility at the embryonic and larval stages, when the innate immune system is already effective. We have thus tested the susceptibility of zebrafish larvae to the human pathogenListeria monocytogenes, a gram-positive, facultative, intracellular bacterium that is known to survive and multiply in professional phagocytes and that causes fatal meningitis and abortions. Intravenous injection of early zebrafish larvae resulted in a progressive and ultimately fatal infection. Blood-borneL. monocytogenesbacteria were quickly trapped and engulfed by macrophages, an event that, for the first time, could be captured in vivo and in real time. Granulocytes also participated in the innate immune response. As in mammals, bacteria could escape the macrophage phagosome in a listeriolysin-dependent manner and accessed the cytosol; this event was critical for bacterial virulence, as listeriolysin-deficient bacteria were completely avirulent. Actin comet tails and protrusions were observed, suggesting cell-to-cell spread; these phenomena also played a role in virulence in zebrafish larvae, asactA-deficient bacteria were attenuated. These results demonstrate the relevance of the genetically tractable and optically accessible zebrafish model for the study ofL. monocytogenespathogenesis and particularly for the dissection of its interactions with phagocytes in vivo, a key factor ofL. monocytogenesvirulence.
Published: 2009

50. Modeling human listeriosis in natural and genetically engineered animals

Author: Olivier Disson, Pascale Cossart, Marc Lecuit, Georgios Nikitas, Olivier Dussurget, and Solène Grayo
Subjects: Genetically modified mouse, Guinea Pigs, Mice, Transgenic, Biology, medicine.disease_cause, General Biochemistry, Genetics and Molecular Biology, Microbiology, Animals, Genetically Modified, Transduction (genetics), Mice, Listeria monocytogenes, Bacterial Proteins, medicine, Animals, Humans, Listeriosis, Receptor, Genetics, Meningoencephalitis, Membrane Proteins, Transfection, medicine.disease, Xenodiagnosis, Disease Models, Animal, Parasitology, biology.protein, Food Microbiology, Antibody, Gerbillinae
Abstract: Listeria monocytogenes causes listeriosis, a human foodborne infection leading to gastroenteritis, meningoencephalitis and maternofetal infections. InlA and InlB, two L. monocytogenes surface proteins, interact with their respective receptors E-cadherin and Met and mediate bacterial entry into human cultured cells. Here, we present protocols for studying listeriosis in three complementary animal models: (i) the human E-cadherin (hEcad) transgenic mouse line; (ii) the knock-in E16P mouse line; and (iii) the gerbil, in which both InlA–E-cadherin and InlB–Met species-specific interactions occur as in humans. Two routes of infection are described: oral inoculation, the natural route for infection; and intravenous inoculation that bypasses the intestinal barrier. We describe how to monitor L. monocytogenes infection, both qualitatively by imaging techniques and quantitatively by bacterial enumeration. The advantage of these methods over the classical intravenous inoculation of L. monocytogenes in wild-type mice (in which the InlA–E-cadherin interaction does not occur) is that it allows the pathophysiology of listeriosis to be studied in animal models relevant to humans, as they are permissive to the interactions that are thought to mediate L. monocytogenes crossing of human host barriers. The whole procedure (inoculation, in vivo imaging, bacterial enumeration, histopathology) takes one full week to complete, including 3 d of actual experiments.
Published: 2009

Catalog

Books, media, physical & digital resources

See catalog results

Searchworks

Select search scope, currently: Articles Catalog books, media & more in Jio Institute collections Articles journal articles & other e-resources

Search

Search Constraints

Refine your results

Search Limiters

Topic

Publication Year Range

Language

Publication Type

Journal

Database

Publisher

60 results on '"Olivier Disson"'

Search Results

Catalog

Select search scope, currently: Articles

Catalog

books, media & more in Jio Institute collections

Articles

journal articles & other e-resources