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4 results on '"immunology [Listeriosis]"'

1. Transmission of trained immunity and heterologous resistance to infections across generations

Author

Gilles Gasparoni, Andreas Schlitzer, Branko Cirovic, Joachim L. Schultze, Didier Le Roy, Kristian Händler, Evangelos J. Giamarellos-Bourboulis, Jorge Domínguez-Andrés, Jörn Walter, Leo A. B. Joosten, Marc Beyer, Jos W. M. van der Meer, Kathrin Kattler, Heidi Theis, Natalie Katzmarski, Mihai G. Netea, Eleonora Ciarlo, Georgios Renieris, Konstantin Lepikhov, and Thierry Roger

Subjects
Male, Heredity, Transcription, Genetic, genetics [Escherichia coli Infections], lnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4], immunology [Escherichia coli], Epigenesis, Genetic, microbiology [Listeriosis], Candida albicans, Immunology and Allergy, Listeriosis, Myeloid Cells, genetics [Listeriosis], Escherichia coli Infections, Cells, Cultured, immunology [Escherichia coli Infections], metabolism [Spermatozoa], biology, immunology [Listeriosis], Effector, Candidiasis, immunology [Listeria monocytogenes], Spermatozoa, pathogenicity [Candida albicans], metabolism [Escherichia coli Infections], immunology [Candidiasis], pathogenicity [Escherichia coli], immunology [Candida albicans], DNA methylation, Host-Pathogen Interactions, Transgene, genetics [Candidiasis], Immunology, Heterologous, Mice, Transgenic, metabolism [Myeloid Cells], Immune system, Immunity, Escherichia coli, Animals, Epigenetics, ddc:610, metabolism [Listeriosis], pathogenicity [Listeria monocytogenes], microbiology [Escherichia coli Infections], microbiology [Candidiasis], DNA Methylation, biology.organism_classification, Listeria monocytogenes, Immunity, Innate, genetics [Immunity, Innate], Disease Models, Animal, microbiology [Myeloid Cells], metabolism [Candidiasis], immunology [Spermatozoa], immunology [Myeloid Cells]
Abstract

Intergenerational inheritance of immune traits linked to epigenetic modifications has been demonstrated in plants and invertebrates. Here we provide evidence for transmission of trained immunity across generations to murine progeny that survived a sublethal systemic infection with Candida albicans or a zymosan challenge. The progeny of trained mice exhibited cellular, developmental, transcriptional and epigenetic changes associated with the bone marrow-resident myeloid effector and progenitor cell compartment. Moreover, the progeny of trained mice showed enhanced responsiveness to endotoxin challenge, alongside improved protection against systemic heterologous Escherichia coli and Listeria monocytogenes infections. Sperm DNA of parental male mice intravenously infected with the fungus C. albicans showed DNA methylation differences linked to immune gene loci. These results provide evidence for inheritance of trained immunity in mammals, enhancing protection against infections. Transgenerational transmission of acquired immunological traits has been demonstrated in invertebrates and plants but not mammals. Katzmarski et al. demonstrate that trained immunity that protects against heterologous infections can be transmitted to F2 offspring.

Published
2021
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2. Distinct surveillance pathway for immunopathology during acute infection via autophagy and SR-BI

Author

Steffen Massberg, Astrid Magenau, Franz Rinninger, Maryana Nichols, Bernd Engelmann, Avinash Khandagale, Harry F. G. Heijnen, Susanne Pfeiler, Katharina Gaus, Tilman Ziegler, Stephanie Seveau, Admar Verschoor, Eicke Latz, Sören Schubert, and Stefan Zahler

Subjects
0301 basic medicine, genetics [Golgi Apparatus], Neutrophils, Golgi Apparatus, Mice, genetics [Splenic Diseases], pathology [Splenic Diseases], Immunopathology, Listeriosis, immunology [Membrane Microdomains], Internalization, genetics [Listeriosis], pathology [Listeriosis], media_common, Mice, Knockout, immunology [Neutrophils], pathology [Neutrophils], Multidisciplinary, immunology [Listeriosis], genetics [Liver Diseases], Liver Diseases, Inflammasome, immunology [Listeria monocytogenes], immunology [Macrophages], genetics [Pinocytosis], Scavenger Receptors, Class B, genetics [Neutrophil Infiltration], Cell biology, Neutrophil Infiltration, symbols, Beclin-1, medicine.drug, immunology [Neutrophil Infiltration], genetics [Autophagy], media_common.quotation_subject, immunology [Beclin-1], Biology, Article, 03 medical and health sciences, symbols.namesake, Immune system, Membrane Microdomains, immunology [Pinocytosis], medicine, Autophagy, Animals, immunology [Liver Diseases], immunology [Scavenger Receptors, Class B], Scavenger receptor, Splenic Diseases, genetics [Membrane Microdomains], immunology [Autophagy], Macrophages, pathology [Liver Diseases], Golgi apparatus, immunology [Golgi Apparatus], Listeria monocytogenes, 030104 developmental biology, immunology [Splenic Diseases], Apoptosis, genetics [Beclin-1], Pinocytosis, Scarb1 protein, mouse, ddc:600, genetics [Scavenger Receptors, Class B], pathology [Macrophages]
Abstract

The mechanisms protecting from immunopathology during acute bacterial infections are incompletely known. We found that in response to apoptotic immune cells and live or dead Listeria monocytogenes scavenger receptor BI (SR-BI), an anti-atherogenic lipid exchange mediator, activated internalization mechanisms with characteristics of macropinocytosis and, assisted by Golgi fragmentation, initiated autophagic responses. This was supported by scavenger receptor-induced local increases in membrane cholesterol concentrations which generated lipid domains particularly in cell extensions and the Golgi. SR-BI was a key driver of beclin-1-dependent autophagy during acute bacterial infection of the liver and spleen. Autophagy regulated tissue infiltration of neutrophils, suppressed accumulation of Ly6C+ (inflammatory) macrophages and prevented hepatocyte necrosis in the core of infectious foci. Perifocal levels of Ly6C+ macrophages and Ly6C− macrophages were unaffected, indicating predominant regulation of the focus core. SR-BI-triggered autophagy promoted co-elimination of apoptotic immune cells and dead bacteria but barely influenced bacterial sequestration and survival or inflammasome activation, thus exclusively counteracting damage inflicted by immune responses. Hence, SR-BI- and autophagy promote a surveillance pathway that partially responds to products of antimicrobial defenses and selectively prevents immunity-induced damage during acute infection. Our findings suggest that control of infection-associated immunopathology can be based on a unified defense operation.

Published
2016
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3. A comparative phenotypic and genomic analysis of C57BL/6J and C57BL/6N mouse strains

Author

Wolfgang Wurst, Elodie Bedu, John M. Hancock, Debra Brooker, Wolfgang Hans, Marie-France Champy, Sarah Atkins, Kim Wong, Martin Hrabě de Angelis, Elisabetta Golini, Karen P. Steel, Oliver Puk, Silvia Mandillo, Abdel Ayadi, George Nicholson, Elizabeth J. Cartwright, Mohammed Selloum, Min Zi, David J. Adams, Pierre Jurdic, Hilary Gates, Hugh P. Morgan, Anna-Karin Gerdin, Steve D.M. Brown, Luis Santos, Petr Danecek, Sabine M. Hölter, Jan Rozman, Mark Sanderson, Helmut Fuchs, Hamid Meziane, Sara Wells, Lore Becker, Binnaz Yalcin, Carl Shannon, Roy Combe, Michelle Simon, Valerie E. Vancollie, Werner Müller, Thomas M. Keane, Valerie Gailus-Durner, Ann-Marie Mallon, Yann Herault, Simon Greenaway, Romain Dacquin, Sophia Djebali, Frédéric Preitner, Frauke Neff, Jacqueline K. White, Ramiro Ramirez-Solis, Tertius Hough, Ian J. Jackson, Anne Southwell, Andreas Lengeling, Neil J. Ingham, Tania Sorg, Michel Roux, Bastian Pasche, Jeanne Estabel, Heather Cater, Laura-Anne Roberson, Glauco P. Tocchini-Valentini, Jochen Graw, Armida Di Fenza, Andrew Blake, Henrik Westerberg, Jacqueline Marvel, Medical Research Council Harwell (Mammalian Genetics Unit and Mary Lyon Centre), Medical Research Counc, The Wellcome Trust Sanger Institute [Cambridge], German Research Centre for Environmental Health, Helmholtz-Zentrum München (HZM), Institut Clinique de la Souris (ICS), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Strasbourg (UNISTRA), Faculty of Medical and Human Sciences, University of Manchester [Manchester], SFR Biosciences, École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Immunité et lymphocytes cytotoxiques – Immunity and cytotoxic lymphocytes, Centre International de Recherche en Infectiologie - UMR (CIRI), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Medical Research Council Human Genetics Unit (IGMM), University of Edinburgh, Infection and Immunity Division, Cell Biology and Neurobiology Institute, Consiglio Nazionale delle Ricerche [Roma] (CNR), Department of Infection Genetics, Helmholtz Centre for Infection Research (HZI), Faculty of Life Sciences, Mouse Metabolic Facility of the Cardiomet Center, Université de Lausanne (UNIL), Chair for Developmental Genetics, Technische Universität Munchen - Université Technique de Munich [Munich, Allemagne] (TUM), Max Planck Institute of Psychiatry, Max-Planck-Gesellschaft, Deutsches Zentrum für Neurodegenerative Erkrankungen, Center for Integrative Genomics - Institute of Bioinformatics, Génopode (CIG), Swiss Institute of Bioinformatics [Lausanne] (SIB), Université de Lausanne (UNIL)-Université de Lausanne (UNIL), The project was funded by the European Commission contract numbers LSHG-CT-2006-037188 EUMODIC and LSHG-CT-2007-037445, and also supported by the Wellcome Trust (grant number 098051)., BMC, Ed., Helmholtz Zentrum München = German Research Center for Environmental Health, Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université de Lausanne = University of Lausanne (UNIL), Université de Lausanne = University of Lausanne (UNIL)-Université de Lausanne = University of Lausanne (UNIL), École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), Centre International de Recherche en Infectiologie (CIRI), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and National Research Council of Italy | Consiglio Nazionale delle Ricerche (CNR)

Subjects
Male, Candidate gene, immunology [Killer Cells, Natural], sequence variation, Mouse Inbred Lines, Sequence Variation, Mouse Phenotyping, Gene Knockout, C57bl/6, C57BL/6, [SDV.GEN] Life Sciences [q-bio]/Genetics, Eye, diagnostic imaging [Femur], Genome, microbiology [Listeriosis], 0302 clinical medicine, Inbred strain, INDEL Mutation, immunology [Hypersensitivity], Listeriosis, Femur, mouse phenotyping, Disease Resistance, Genetics, pathology [Eye], 0303 health sciences, Behavior, Animal, immunology [Listeriosis], Killer Cells, Natural, Phenotype, genetics [Polymorphism, Single Nucleotide], [SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Female, genetics [Genome], Mouse inbred lines, gene knockout, Biology, Polymorphism, Single Nucleotide, immunology [Spleen], International Knockout Mouse Consortium, 03 medical and health sciences, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], ddc:570, Hypersensitivity, Animals, Expressivity (genetics), genetics [INDEL Mutation], immunology [Disease Resistance], Maze Learning, Gene, 030304 developmental biology, Whole genome sequencing, [SDV.GEN]Life Sciences [q-bio]/Genetics, Research, X-Ray Microtomography, Mouse inbred lines sequence variation mouse phenotyping gene knockout C57BL/6 sequencing data complex traits gene-function resource mice europhenome annotation substrains variants database, Human genetics, Mice, Inbred C57BL, 030217 neurology & neurosurgery, Spleen
Abstract

International audience; BACKGROUND: The mouse inbred line C57BL/6J is widely used in mouse genetics and its genome has been incorporated into many genetic reference populations. More recently large initiatives such as the International Knockout Mouse Consortium (IKMC) are using the C57BL/6N mouse strain to generate null alleles for all mouse genes. Hence both strains are now widely used in mouse genetics studies. Here we perform a comprehensive genomic and phenotypic analysis of the two strains to identify differences that may influence their underlying genetic mechanisms. RESULTS: We undertake genome sequence comparisons of C57BL/6J and C57BL/6N to identify SNPs, indels and structural variants, with a focus on identifying all coding variants. We annotate 34 SNPs and 2 indels that distinguish C57BL/6J and C57BL/6N coding sequences, as well as 15 structural variants that overlap a gene. In parallel we assess the comparative phenotypes of the two inbred lines utilizing the EMPReSSslim phenotyping pipeline, a broad based assessment encompassing diverse biological systems. We perform additional secondary phenotyping assessments to explore other phenotype domains and to elaborate phenotype differences identified in the primary assessment. We uncover significant phenotypic differences between the two lines, replicated across multiple centers, in a number of physiological, biochemical and behavioral systems. CONCLUSIONS: Comparison of C57BL/6J and C57BL/6N demonstrates a range of phenotypic differences that have the potential to impact upon penetrance and expressivity of mutational effects in these strains. Moreover, the sequence variants we identify provide a set of candidate genes for the phenotypic differences observed between the two strains.

Published
2013
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4. Cell biology. Sheddase gets guidance

Author

Lichtenthaler, Stefan

Subjects
Lipopolysaccharides, immunology [Listeriosis], Tumor Necrosis Factor-alpha, metabolism [Tumor Necrosis Factor-alpha], ADAM17 Protein, Immunity, Innate, ADAM Proteins, metabolism [ADAM Proteins], ddc:320, iRhom2 protein, mouse, Animals, Humans, immunology [Lipopolysaccharides], immunology [Shock, Septic], Carrier Proteins, metabolism [Carrier Proteins], Signal Transduction
Published
2012
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