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4. Lésions inflammatoires cutanées de type Th1 chez un patient atteint de pseudoxanthome élastique

Author

Rocour, S., Vinatier, E., Fassot, C., Dauvé, J., Le Saux, O., Morel, A., Delneste, Y., and Martin, L.

Abstract

Le pseudoxanthome élastique (PXE) est une maladie héréditaire du tissu conjonctif caractérisée par une calcification ectopique des tissus riches en fibres élastiques (OMIM 264 800). Le PXE est actuellement considéré comme une pathologie de la calcification. Des données récentes suggèrent l’existence d’une composante inflammatoire au cours du PXE (augmentation de la captation du 18F-FDG, altération du flux sanguin microvasculaire dans les zones affectées…). Nous avons eu l’opportunité d’investiguer un jeune patient qui présentait des poussées érythémateuses de ses lésions cutanées de PXE, phénomène rarement rencontré en pratique clinique.

Published
2024
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5. Mycolactone toxin induces an inflammatory response by targeting the IL-1β pathway: Mechanistic insight into Buruli ulcer pathophysiology

Author

Foulon, M, Robbe-Saule, M, Manry, J, Esnault, L, Boucaud, Y, Alcaïs, A, Malloci, M, Fanton D’andon, M, Beauvais, T, Labarrière, Nathalie, Jeannin, P, Abel, L, Saint-André, J, Croué, A, Delneste, Y, Boneca, I, Marsollier, L, Marion, E, ATOMycA (CRCINA-ÉQUIPE 6), Centre de Recherche en Cancérologie et Immunologie Nantes-Angers (CRCINA), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA), Human genetics of infectious diseases : Mendelian predisposition (Equipe Inserm U1163), Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), Plateforme MicroPicell [Nantes], Université de Nantes (UN), Biologie et Génétique de la Paroi bactérienne - Biology and Genetics of Bacterial Cell Wall, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Anti-Tumor Immunosurveillance and Immunotherapy (CRCINA-ÉQUIPE 3), LabEX IGO Immunothérapie Grand Ouest, Innate Immunity and Immunotherapy (CRCINA-ÉQUIPE 7), Laboratoire d'Immunologie et d'Allergologie [CHU Angers], Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM)-PRES Université Nantes Angers Le Mans (UNAM), Département de Pathologie Cellulaire et Tissulaire [CHU Angers], Université d'Angers (UA)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Université d'Angers (UA)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Nantes Université (Nantes Univ), ANR-16-CE12-0023,MYCOPARADOX,Dissection de l'architecture génétique des réactions paradoxales dans la Lèpre et l'Ulcère de Buruli(2016), and LABARRIERE, Nathalie

Subjects
Bacterial Diseases, Physiology, Interleukin-1beta, [SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunity, White Blood Cells, Mice, Medical Conditions, Animal Cells, Medicine and Health Sciences, Biology (General), Buruli Ulcer, Immune Response, Gene Ontologies, Genomics, Actinobacteria, Infectious Diseases, Macrolides, Cellular Types, Cellular Structures and Organelles, [SDV.MP.PAR] Life Sciences [q-bio]/Microbiology and Parasitology/Parasitology, Research Article, Neglected Tropical Diseases, QH301-705.5, Immune Cells, Immunology, Extracellular Vesicles, Signs and Symptoms, Genetics, Animals, Humans, [SDV.MP.PAR]Life Sciences [q-bio]/Microbiology and Parasitology/Parasitology, Vesicles, [SDV.IMM.II] Life Sciences [q-bio]/Immunology/Innate immunity, Secretion, Inflammation, Blood Cells, Bacteria, Mycobacterium ulcerans, Macrophages, Organisms, Biology and Life Sciences, Computational Biology, Cell Biology, RC581-607, Tropical Diseases, Genome Analysis, Mice, Inbred C57BL, Lesions, Clinical Medicine, Immunologic diseases. Allergy, Physiological Processes
Abstract

Mycolactone, a lipid-like toxin, is the major virulence factor of Mycobacterium ulcerans, the etiological agent of Buruli ulcer. Its involvement in lesion development has been widely described in early stages of the disease, through its cytotoxic and immunosuppressive activities, but less is known about later stages. Here, we revisit the role of mycolactone in disease outcome and provide the first demonstration of the pro-inflammatory potential of this toxin. We found that the mycolactone-containing mycobacterial extracellular vesicles produced by M. ulcerans induced the production of IL-1β, a potent pro-inflammatory cytokine, in a TLR2-dependent manner, targeting NLRP3/1 inflammasomes. We show our data to be relevant in a physiological context. The in vivo injection of these mycolactone-containing vesicles induced a strong local inflammatory response and tissue damage, which were prevented by corticosteroids. Finally, several soluble pro-inflammatory factors, including IL-1β, were detected in infected tissues from mice and Buruli ulcer patients. Our results revisit Buruli ulcer pathophysiology by providing new insight, thus paving the way for the development of new therapeutic strategies taking the pro-inflammatory potential of mycolactone into account., Author summary Buruli ulcer is a neglected tropical disease occurring mainly in poor rural areas of West and Central Africa. This cutaneous disease is caused by Mycobacterium ulcerans, a bacterium belonging to the same family as M. tuberculosis and M. leprae. The skin lesions are caused by a cytotoxic toxin named mycolactone, also known to act as an immunosuppressor and an anti-inflammatory molecule. However, Buruli ulcer lesions are characterized by a chronic cutaneous inflammation with a recruitment of cellular immune cells trying to counteract M. ulcerans. Our work allows for a reconcilitation of previous observations. We found by in vitro experiment on macrophages that the mycolactone-containing mycobacterial extracellular vesicles produced by M. ulcerans induced the production of IL-1β, a potent pro-inflammatory molecule, while other pro-inflammatory soluble factors are inhibited. We also detected IL-1β protein in a mouse model of M. ulcerans infection as well as in biopsies of Buruli ulcer patients. The pro-inflammatory potential of mycolacone has to be taken into account to understand the full pathophysiology of Buruli ulcer.

Published
2020
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7. Functional foods: mechanisms of action on immunocompetent cells

Author

Delneste, Y., Donnet-Hughes, A., and Schiffrin, E.J.

Subjects
Enterobacteriaceae -- Research, Intestines -- Microbiology, Immunocompetent cells -- Health aspects, Lactobacillus -- Physiological aspects, Food/cooking/nutrition
Abstract

Lactic acid bacteria strains and comensal enterobacteria are compared for their immunologic effects on human enterocytes. This research helps to understand how intestinal microflora affect the homeostasis of the mucosal immune system against infection.

Published
1998

14. Clusterin facilitates apoptotic cell clearance and prevents apoptotic cell-induced autoimmune responses

Author

Cunin, P, Beauvillain, C, Miot, C, Augusto, J-F, Preisser, L, Blanchard, S, Pignon, P, Scotet, M, Garo, E, Fremaux, I, Chevailler, A, Subra, J, Blanco, P, Wilson, Mark R, Jeannin, Pascale, Delneste, Y, Cunin, P, Beauvillain, C, Miot, C, Augusto, J-F, Preisser, L, Blanchard, S, Pignon, P, Scotet, M, Garo, E, Fremaux, I, Chevailler, A, Subra, J, Blanco, P, Wilson, Mark R, Jeannin, Pascale, and Delneste, Y

Abstract

Clusterin (Clu), an extracellular chaperone, exhibits characteristics of soluble innate immunity receptors, as assessed by its ability to bind some bacteria strains. In this study, we report that Clu also binds specifically to late apoptotic cells but not to live, early apoptotic, or necrotic cells. Histones, which accumulate on blebs during the apoptotic process, represent privileged Clu-binding motifs at the surface of late apoptotic cells. As a consequence, Clu potentiates, both in vitro and in vivo, the phagocytosis of late apoptotic cells by macrophages. Moreover, the increased phagocytosis of late apoptotic cells induced by Clu favors the presentation and cross-presentation of apoptotic cell-associated antigens. Finally, we observed that, in a model of apoptotic cell-induced autoimmunity, and relative to control mice, Clu-/- mice develop symptoms of autoimmunity, including the generation of anti-dsDNA antibodies, deposition of immunoglobulins and complement components within kidneys, and splenomegaly. These results identify Clu as a new molecule partner involved in apoptotic cell efferocytosis and suggest a protective role for Clu in inflammation and autoimmune diseases.

Published
2016

15. Clusterin facilitates apoptotic cell clearance and prevents apoptotic cell-induced autoimmune responses

Author

Cunin, P, primary, Beauvillain, C, additional, Miot, C, additional, Augusto, J-F, additional, Preisser, L, additional, Blanchard, S, additional, Pignon, P, additional, Scotet, M, additional, Garo, E, additional, Fremaux, I, additional, Chevailler, A, additional, Subra, J-F, additional, Blanco, P, additional, Wilson, M R, additional, Jeannin, P, additional, and Delneste, Y, additional

Published
2016
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16. Blockade of angiotensin II type 2 receptor delays early tumorigenesis by inhibiting tumor cell proliferation and angiogenesis

Author

Clere, N., Corre, I., Faure, S., Guihot, A. L., Vessieres, E., Chalopin, M., Morel, A., Olivier Coqueret, Hein, L., Delneste, Y., Paris, F., Henrion, D., Stress Oxydant et Pathologies Métaboliques (SOPAM), Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherche en Cancérologie Nantes-Angers (CRCNA), Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM)-PRES Université Nantes Angers Le Mans (UNAM)-Hôtel-Dieu de Nantes-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hôpital Laennec-Centre National de la Recherche Scientifique (CNRS)-Faculté de Médecine d'Angers-Centre hospitalier universitaire de Nantes (CHU Nantes), Biologie Neurovasculaire Intégrée (BNVI), Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Laboratoire méditerranéen de préhistoire Europe-Afrique (LAMPEA), Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS)-Ministère de la Culture (MC), Dynamique sociétés-environnements sur le temps long en Afrique périsaharienne, Biologie Neurovasculaire et Mitochondriale Intégrée (BNMI), and Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université d'Angers (UA)

Subjects
[SDV]Life Sciences [q-bio]
Abstract

Whereas the angiotensin II type 2 receptor (AT2R) is known to oppose the proliferative and growth properties of the type 1 receptor, its role in pathological conditions may be different. Although it is highly expressed in cancer cells, its role in tumor progression remains poorly understood. We aimed to investigate the involvement of the AT2R in early tumorigenesis hypothesizing that it may affect tumor cell proliferation and/or tumor angiogenesis. Tumors were induced with 3-methylcholanthrene (3-MCA, 20 mg/kg, s.c.) in FVB/N mice lacking the AT2R (AT2R-KO) or through LL/2 cells injection in C57/BL6N mice treated with the AT2R antagonist PD123,319. Cell proliferation was evaluated by Ki-67 immunochemistry. Vascular density was determined using CD31 labelling and angiogenesis was measured using the aortic ring assay. Tumor initiation by 3-MCA was significantly delayed in AT2R-KO compared to wild type mice (56 days vs 28 days).Tumorigenesis following LL/2 cells injection in C57BL/6N mice was significantly reduced then the AT2R antagonist PD123,319 was given at an early stage of tumor development, suggesting a role of AT2R in tumor promotion. Moreover, in vitro proliferation of LL/2 cells was reduced by PD123,319 with a significant decrease in Ki-67 expression, a marker of cell proliferation. Tumor microvascular density and angiogenesis were significantly reduced in wild type mice treated with PD123,319 and in AT2R-null mice, compared to control animals. Thus, we showed that the AT2R has a key role in tumor development, favouring both malignant cell proliferation and tumor angiogenesis.

Published
2009
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18. Regulation of Mycolactone, the Mycobacterium ulcerans Toxin, Depends on Nutrient Source

Author

Phillips, RO, Deshayes, C, Angala, SK, Marion, E, Brandli, I, Babonneau, J, Preisser, L, Eyangoh, S, Delneste, Y, Legras, P, De Chastellier, C, Stinear, TP, Jackson, M, Marsollier, L, Phillips, RO, Deshayes, C, Angala, SK, Marion, E, Brandli, I, Babonneau, J, Preisser, L, Eyangoh, S, Delneste, Y, Legras, P, De Chastellier, C, Stinear, TP, Jackson, M, and Marsollier, L

Abstract

Background Mycobacterium ulcerans, a slow-growing environmental bacterium, is the etiologic agent of Buruli ulcer, a necrotic skin disease. Skin lesions are caused by mycolactone, the main virulence factor of M. ulcerans, with dermonecrotic (destruction of the skin and soft tissues) and immunosuppressive activities. This toxin is secreted in vesicles that enhance its biological activities. Nowadays, it is well established that the main reservoir of the bacilli is localized in the aquatic environment where the bacillus may be able to colonize different niches. Here we report that plant polysaccharides stimulate M. ulcerans growth and are implicated in toxin synthesis regulation. Methodology/Principal Findings In this study, by selecting various algal components, we have identified plant-specific carbohydrates, particularly glucose polymers, capable of stimulating M. ulcerans growth in vitro. Furthermore, we underscored for the first time culture conditions under which the polyketide toxin mycolactone, the sole virulence factor of M. ulcerans identified to date, is down-regulated. Using a quantitative proteomic approach and analyzing transcript levels by RT-qPCR, we demonstrated that its regulation is not at the transcriptional or translational levels but must involve another type of regulation. M. ulcerans produces membrane vesicles, as other mycobacterial species, in which are the mycolactone is concentrated. By transmission electron microscopy, we observed that the production of vesicles is independent from the toxin production. Concomitant with this observed decrease in mycolactone production, the production of mycobacterial siderophores known as mycobactins was enhanced. Conclusions/Significance This work is the first step in the identification of the mechanisms involved in mycolactone regulation and paves the way for the discovery of putative new drug targets in the future.

Published
2013

19. A novel matrilysin like proteinase

Author

De Coignac A, Benoit, Elson, G., Delneste, Y., Magistralli, G., Jannin, Pierre, J. P., Aubry, Berthier-Vergnes, O., Schmitt, D., J. Y., Bonnefoy, J. F., Gauchat, Centre de génétique et de physiologie moléculaire et cellulaire (CGPhiMC), Centre National de la Recherche Scientifique (CNRS)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon, and Laviron, Nathalie

Subjects
[SDV.BC]Life Sciences [q-bio]/Cellular Biology, [SDV.BC] Life Sciences [q-bio]/Cellular Biology
Published
2000

20. Cloning of MMP-26 : a novel matrilysin like proteinase

Author

de Coignac A, Benoit, Elson, G., Delneste, Y., Magristralli, G., Jeannin, P., Jp, Aubry, Berthier-Vergnes, O., Schmitt, D., J. Y., Bonnefoy, Jf, Gauchat, and Laviron, Nathalie

Subjects
[SDV.BC] Life Sciences [q-bio]/Cellular Biology
Published
2000

21. P149 Role of the humoral pattern recognition molecule PTX3 in defence against urinary tract infections

Author

Jaillon, S., primary, Moalli, F., additional, Ragnarsdottir, B., additional, Bonavita, E., additional, Riva, F., additional, Barbati, E., additional, Nebuloni, M., additional, Valentino, S., additional, Graziani, G., additional, Montanelli, A., additional, Delneste, Y., additional, Svanborg, C., additional, Garlanda, C., additional, and Mantovani, A., additional

Published
2012
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49. Endogenous PTX3 translocates at the membrane of late apoptotic human neutrophils and is involved in their engulfment by macrophages.

Author

Jaillon, S., Jeannin, P., Hamon, Y., Frémaux, I., Doni, A., Bottazzi, B., Blanchard, S., Subra, J.-F., Chevailler, A., Mantovani, A., and Delneste, Y.

Subjects
NEUTROPHILS, APOPTOSIS, MACROPHAGES, AUTOIMMUNITY, GRANULOCYTES
Abstract

Neutrophils are short-lived innate immune cells that rapidly die by apoptosis. A rapid and efficient clearance of apoptotic cells is crucial to avoid autoimmunity. This process involves cell alterations, endocytic receptors expressed by phagocytic cells and soluble bridging molecules (opsonins) that facilitate internalization of apoptotic cells by phagocytes. Neutrophils constitutively express the prototypic long pentraxin PTX3 that binds to apoptotic cells and modulates their clearance. We thus evaluated whether endogenous PTX3 may interfere with the capture of apoptotic neutrophils. We observed that PTX3 accumulates in blebs at the surface of late apoptotic neutrophils, resulting from its active translocation from granules to the membrane. A neutralizing anti-PTX3 monoclonal Ab (mAb) inhibits the capture of late apoptotic neutrophils by macrophages. This study shows that intracellular PTX3 translocates at the surface of late apoptotic neutrophils and acts as an ‘eat-me’ molecule for their recognition and capture by macrophages.Cell Death and Differentiation (2009) 16, 465–474; doi:10.1038/cdd.2008.173; published online 12 December 2008 [ABSTRACT FROM AUTHOR]

Published
2009
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