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5 results on '"Inflammation intestinale pathologique de l'enfant"'

1. Yersinia pseudotuberculosis Effector YopJ Subverts the Nod2/RICK/TAK1 Pathway and Activates Caspase-1 to Induce Intestinal Barrier Dysfunction

Author

Frédérick Barreau, Maryline Roy, Claude Villard, Monique Dussaillant, Jean-Pierre Hugot, Sophie Esmiol-Welterlin, Dominique Berrebi, Hans Wolf-Watz, Ulrich Meinzer, Thibaut Léger, Ziad Alnabhani, Vincent Ollendorff, Sanah Ben-Mkaddem, Camille Jung, Stéphane Bonacorsi, Julie Perroy, Centre de recherche clinique, Hôpital intercommunal de Créteil, Institut de biologie et chimie des protéines [Lyon] (IBCP), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS), Institut Jacques Monod (IJM (UMR_7592)), Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), U996 DHU Hépatinov, Université Paris Sud (Paris 11), UMR 843 Inflammation intestinale pathologique de l'enfant, Institut National de la Santé et de la Recherche Médicale (INSERM), CRI UMR 1149, Lab Excellence Inflamex, Université Paris Diderot - Paris 7 (UPD7), AP-HP Hôpital universitaire Robert-Debré [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut de Génomique Fonctionnelle (IGF), Université de Montpellier (UM)-Université Montpellier 1 (UM1)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Montpellier 2 - Sciences et Techniques (UM2)-Centre National de la Recherche Scientifique (CNRS), Dynamique Musculaire et Métabolisme (DMEM), Institut National de la Recherche Agronomique (INRA)-Université de Montpellier (UM), Origine, structure et évolution de la biodiversité (OSEB), Muséum national d'Histoire naturelle (MNHN)-Centre National de la Recherche Scientifique (CNRS), Université de Montpellier (UM)-Institut National de la Recherche Agronomique (INRA), Origine, structure et évolution de la biodiversité, Centre National de la Recherche Scientifique (CNRS), and Université Montpellier 1 (UM1)-Université Montpellier 2 - Sciences et Techniques (UM2)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Male, Cancer Research, Caspase 1, Nod2 Signaling Adaptor Protein, Yersinia pseudotuberculosis Infections, Yersinia, Microbiology, Cell Line, 03 medical and health sciences, Mice, Bacterial Proteins, Receptor-Interacting Protein Serine-Threonine Kinase 2, Virology, NOD2, Immunology and Microbiology(all), Yersinia pseudotuberculosis, Animals, Humans, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Intestinal Mucosa, Molecular Biology, ComputingMilieux_MISCELLANEOUS, 030304 developmental biology, 0303 health sciences, Innate immune system, biology, Effector, Kinase, 030302 biochemistry & molecular biology, biology.organism_classification, MAP Kinase Kinase Kinases, digestive system diseases, Intestines, Mice, Inbred C57BL, Parasitology, Female, Signal transduction, Signal Transduction
Abstract

International audience; Yersinia pseudotuberculosis is an enteropathogenic bacteria that disrupts the intestinal barrier and invades its host through gut-associated lymphoid tissue and Peyer's patches (PP). We show that the Y. pseudotuberculosis effector YopJ induces intestinal barrier dysfunction by subverting signaling of the innate immune receptor Nod2, a phenotype that can be reversed by pretreating with the Nod2 ligand muramyl-dipeptide. YopJ, but not the catalytically inactive mutant YopJ(C172A), acetylates critical sites in the activation loops of the RICK and TAK1 kinases, which are central mediators of Nod2 signaling, and decreases the affinity of Nod2 for RICK. Concomitantly, Nod2 interacts with and activates caspase-1, resulting in increased levels of IL-1β. Finally, IL-1β within PP plays an essential role in inducing intestinal barrier dysfunction. Thus, YopJ alters intestinal permeability and promotes the dissemination of Yersinia as well as commensal bacteria by exploiting the mucosal inflammatory response.

Published
2012
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2. Altered gut microbiota composition in immune-impaired Nod2(-/-) mice

Author

Joël Doré, Marion Leclerc, Stanislas Mondot, Frédérick Barreau, Ziad Al Nabhani, Karine Le Roux, Patricia Lepage, Jean-Pierre Hugot, Monique Dussaillant, MICrobiologie de l'ALImentation au Service de la Santé (MICALIS), Institut National de la Recherche Agronomique (INRA)-AgroParisTech, UMR 843 Inflammation intestinale pathologique de l'enfant, and Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
[SDV.SA]Life Sciences [q-bio]/Agricultural sciences, Firmicutes, medicine.drug_class, Antibiotics, Nod2 Signaling Adaptor Protein, Ileum, Gut flora, Microbiology, 03 medical and health sciences, 0302 clinical medicine, Immune system, Crohn Disease, NOD2, RNA, Ribosomal, 16S, medicine, Animals, Humans, Feces, 030304 developmental biology, 0303 health sciences, biology, Bacteria, digestive, oral, and skin physiology, Gastroenterology, Bacteroidetes, biology.organism_classification, digestive system diseases, medicine.anatomical_structure, Metagenome, 030211 gastroenterology & hepatology
Abstract

We read with great interest the recently published study by Rehman and colleagues.1 Investigating microbial diversity on faecal and ileal samples from 48 mice using Sanger and 454 techniques, Rehman et al detected increased percentages of Bacteroidetes in the faeces of adult Nod2 −/− mice, whereas Firmicutes levels were significantly higher only in the ileum of Nod2 −/− mice. Since we demonstrated that antibiotic …

Published
2011
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3. Differential expression and regulation of ADAM17 and TIMP3 in acute inflamed intestinal epithelia

Author

Abakar Abakar-Mahamat, Alain Doglio, Eric Selva, Sandra Lassalle, Paul Hofman, Patrick Brest, Jérôme Filippi, Philippe Naquet, Franck Galland, Annabelle Cesaro, Baharia Mograbi, Xavier Hébuterne, Valérie Vouret-Craviari, Jean-Pierre Hugot, Infection bactérienne, inflammation, et carcinogenèse digestive, Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-IFR50-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Côte d'Azur (UCA), Immunité muqueuse et vaccination, Inflammation intestinale pathologique de l'enfant, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre d'Immunologie de Marseille - Luminy (CIML), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Nice Sophia Antipolis (... - 2019) (UNS), and COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-IFR50-Université Côte d'Azur (UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
Physiology, Colon, Neutrophils, Neutrophile, Biopsy, Nod2 Signaling Adaptor Protein, Gene Expression, Biology, ADAM17 Protein, Tight Junctions, 03 medical and health sciences, 0302 clinical medicine, Crohn Disease, Cell Movement, Ileum, Physiology (medical), Cell Line, Tumor, medicine, Humans, Intestinal Mucosa, 030304 developmental biology, Inflammation, Tissue Inhibitor of Metalloproteinase-3, 0303 health sciences, Crohn's disease, Hepatology, medicine.diagnostic_test, Tumor Necrosis Factor-alpha, Gastroenterology, Antibodies, Monoclonal, Epithelial Cells, Hydrogen Peroxide, medicine.disease, Colitis, Epithelium, N-Formylmethionine Leucyl-Phenylalanine, ADAM Proteins, medicine.anatomical_structure, Gene Expression Regulation, Cell culture, 030220 oncology & carcinogenesis, Immunology, biology.protein, [SDV.IMM]Life Sciences [q-bio]/Immunology, Tumor necrosis factor alpha, Antibody
Abstract

The acute phase of Crohn's disease (CD) is characterized by a large afflux of polymorphonuclear leukocytes (PMNL) into the mucosa and by the release of TNF-α. Conversion of inactive TNF-α into an active form requires the cleavage of a transmembrane TNF-α precursor by the TNF-α-converting enzyme (ADAM17), a protease mainly regulated by the tissue inhibitor of metalloproteinase 3 (TIMP3). The aim of the present study was to investigate in an in vitro model of PMNL transepithelial migration and in the intestinal mucosa of patients with CD the expression and regulation of ADAM17 and TIMP3 in intestinal epithelial cells (IEC). ADAM17 and TIMP3 expression was analyzed by Western blotting, RT-PCR, confocal microscopy, and immunohistochemistry by using the T84 model and digestive biopsies. ADAM17 expression in IEC was increased at a posttranscriptional level during the early phase (from 2 to 4 h) of PMNL transepithelial migration whereas TIMP3 was only increased 24 h later. TNF-α induced an early upregulation of ADAM17 in T84 cells, whereas PMNL adhesion, H2O2, or epithelial tight junction opening alone did not affect the amount of ADAM17. Immunohistochemistry of intestinal biopsies revealed that strong expression of ADAM17 was associated with a high activity of CD. In contrast, TIMP3 was very poorly expressed in these biopsies. ADAM17 and TIMP3 profiling did not correlated with the NOD2/CARD15 status. The ADAM17 activity was higher both in the early phase of PMNL transepithelial migration and in active CD. These results showed early posttranscriptional upregulation of ADAM17 in IEC linked to PMNL transepithelial migration and a high activity of CD.

Published
2009
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4. NOD2: a potential target for regulating liver injury

Author

Jean-Pierre Hugot, Philippe Mathurin, Sylvie Hudault, Sébastien Dharancy, Laurent Dubuquoy, Mathias Chamaillard, Filomena Conti, Pierre Desreumaux, Irene Garcia, Alexandre Louvet, Dominique Berrebi, Emilie Gantier, Philippe J. Sansonetti, Dana J. Philpott, Fabrice Chareyre, Mathilde Body-Malapel, Gilles Pagès, Marco Giovannini, Stephen E. Girardin, Physiopathologie des Maladies Inflammatoires de l'Intestin, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, Droit et Santé, Université de Lille, Droit et Santé, Hôpital Duriez, Service des Maladies de l'Appareil digestif et de la Nutrition, Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Service d'Anatomie et de Cytologie Pathologiques, Hôpital Robert Debré, Inflammation intestinale pathologique de l'enfant, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Immunology, University of Toronto, Génomique Fonctionnelle des Tumeurs Solides (U1162), Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut de signalisation, biologie du développement et cancer (ISBDC), Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA), Department of Laboratory Medicine and Pathobiology (LMP), Université de Genève = University of Geneva (UNIGE), Pathogenes et Fonctions des Cellules Epitheliales Polarisees, Université Paris-Sud - Paris 11 (UP11)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire de Biologie Cellulaire, Université Paris Descartes - Paris 5 (UPD5), Pathogénie Microbienne Moléculaire, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Collège de France - Chaire Microbiologie et Maladies infectieuses, Collège de France (CdF (institution)), Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université de Lille, Droit et Santé, Centre Hospitalier Régional Universitaire [Lille] ( CHRU Lille ), Université Paris Diderot - Paris 7 ( UPD7 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Genomique Fonctionnelle des Tumeurs Solides, Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université Paris Descartes - Paris 5 ( UPD5 ) -IFR105-Université Paris Diderot - Paris 7 ( UPD7 ), Institut de signalisation, biologie du développement et cancer ( ISBDC ), Université Nice Sophia Antipolis ( UNS ), Université Côte d'Azur ( UCA ) -Université Côte d'Azur ( UCA ) -Centre National de la Recherche Scientifique ( CNRS ), Department of Laboratory Medicine and Pathobiology ( LMP ), Department of Pathology and Immunology, Univ. Geneva, University of Geneva [Switzerland], Université Paris-Sud - Paris 11 ( UP11 ) -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 ), Université Nice Sophia Antipolis (... - 2019) (UNS), Université Côte d'Azur (UCA)-Université Côte d'Azur (UCA)-Centre National de la Recherche Scientifique (CNRS), Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre National de la Recherche Scientifique (CNRS)-Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Université Côte d'Azur (UCA), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur [Paris], and Chaire Microbiologie et Maladies infectieuses

Subjects
MESH : RNA, Messenger, MESH: Spleen, Lymphocyte, Nod2 Signaling Adaptor Protein, RNA, Messenger/metabolism, MESH: Adjuvants, Immunologic, Apoptosis, MESH : Hepatocytes, ddc:616.07, MESH : Nod2 Signaling Adaptor Protein, Interferon-gamma/analysis/pharmacology, [ SDV.CAN ] Life Sciences [q-bio]/Cancer, MESH: Hepatocytes, Mice, 0302 clinical medicine, Concanavalin A, MESH: Up-Regulation, MESH: Nod2 Signaling Adaptor Protein, MESH: Animals, MESH : Up-Regulation, MESH : Acetylmuramyl-Alanyl-Isoglutamine, Cells, Cultured, Liver injury, 0303 health sciences, Leukocytes, Mononuclear/drug effects/*immunology, MESH: Hepatitis, Animal, MESH : Interferon Type II, MESH: Case-Control Studies, 3. Good health, Up-Regulation, Acetylmuramyl-Alanyl-Isoglutamine/pharmacology, 030220 oncology & carcinogenesis, Hepatocytes/drug effects/metabolism/physiology, Muramyl dipeptide, MESH: Cells, Cultured, MESH : Case-Control Studies, Liver/*injuries, [ SDV.BBM.BM ] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, MESH: Concanavalin A, Nod2 Signaling Adaptor Protein/analysis/*deficiency/genetics/*metabolism, Pathology and Forensic Medicine, Interferon-gamma, 03 medical and health sciences, Adjuvants, Immunologic, Humans, RNA, Messenger, Molecular Biology, MESH: Humans, Tumor Necrosis Factor-alpha, MESH : Humans, [SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, medicine.disease, digestive system diseases, Immunity, Innate, MESH : Leukocytes, Mononuclear, Mice, Inbred C57BL, chemistry, MESH: Tumor Necrosis Factor-alpha, Case-Control Studies, Immunology, Hepatitis, Animal/chemically induced/*immunology/metabolism/pathology, Leukocytes, Mononuclear, MESH : Hepatitis, Animal, MESH : Apoptosis, MESH: Liver, MESH : Immunity, Natural, Cell Separation, Hepatitis, Animal, MESH: Mice, Knockout, chemistry.chemical_compound, Adjuvants, Immunologic/pharmacology, NOD2, MESH : Concanavalin A, Tumor Necrosis Factor-alpha/analysis/pharmacology, MESH : Tumor Necrosis Factor-alpha, Mice, Knockout, MESH: Kinetics, Concanavalin A/toxicity, MESH: Leukocytes, Mononuclear, medicine.anatomical_structure, Liver, medicine.symptom, MESH : Kinetics, Acetylmuramyl-Alanyl-Isoglutamine, Cell Separation/methods, MESH : Spleen, MESH: Interferon Type II, Inflammation, [SDV.CAN]Life Sciences [q-bio]/Cancer, chemical and pharmacologic phenomena, MESH : Mice, Inbred C57BL, Biology, MESH: Cell Separation, Immune system, MESH: Mice, Inbred C57BL, MESH : Mice, MESH : Cells, Cultured, medicine, Animals, Spleen/cytology/drug effects, MESH: Mice, 030304 developmental biology, MESH: RNA, Messenger, MESH: Immunity, Natural, Hepatitis, Innate immune system, MESH: Apoptosis, MESH : Liver, Cell Biology, Kinetics, MESH: Acetylmuramyl-Alanyl-Isoglutamine, MESH : Cell Separation, Hepatocytes, MESH : Adjuvants, Immunologic, MESH : Mice, Knockout, MESH : Animals, Spleen
Abstract

The recent discovery of bacterial receptors such as NOD2 that contribute to crosstalk between innate and adaptive immune systems in the digestive tract constitutes an important challenge in our understanding of liver injury mechanisms. The present study focuses on NOD2 functions during liver injury. NOD2, TNF-alpha and IFN-gamma mRNA were quantified using real-time PCR in liver samples from patients and mice with liver injury. We evaluated the susceptibility of concanavalin A (ConA) challenge in NOD2-deficient mice (Nod2-/-) compared to wild-type littermates. We tested the effect of muramyl dipeptide (MDP), the specific activator of NOD2, on ConA-induced liver injury in C57BL/6 mice. We studied the cellular distribution and the role of NOD2 in immune cells and hepatocytes. We demonstrated that NOD2, TNF-alpha and IFN-gamma were upregulated during liver injury in mice and humans. Nod2-/- mice were resistant to ConA-induced hepatitis compared to their wild-type littermates, through reduced IFN-gamma production by immune cells. Conversely, administration of MDP exacerbated ConA-induced liver injury. MDP was a strong inducer of IFN-gamma in freshly isolated human PBMC, splenocytes and hepatocytes. Our study supports the hypothesis that NOD2 contributes to liver injury via a regulatory mechanism affecting immune cells infiltrating the liver and hepatocytes. Taken together, our results indicate that NOD2 may represent a new therapeutic target in liver diseases.

Published
2008
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5. Nod2 mediates susceptibility to Yersinia pseudotuberculosis in mice

Author

Thécla Lesuffleur, Stéphane Bonacorsi, Fabrice Chareyre, Hans Wolf-Watz, Ghislaine Sterkers, Michael Karin, Claude Villard, Michel Peuchmaur, Marco Giovannini, Sophie Esmiol-Welterlin, Frédérick Barreau, Vincent Ollendorff, Michiko Niwa-Kawakita, Ulrich Meinzer, Lars Eckmann, Corinne Alberti, Jean-Pierre Hugot, Monique Dussaillant, Dominique Berrebi, Inflammation intestinale pathologique de l'enfant, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Umea Plant Science Centre, Umeå University, Différenciation Cellulaire et Croissance (DCC), Institut National de la Recherche Agronomique (INRA)-Université Montpellier 2 - Sciences et Techniques (UM2), Centre National de la Recherche Scientifique (CNRS), Pathologie pédiatrique (EA_3102), Hôpital Robert Debré-Université Paris Diderot - Paris 7 (UPD7)-IFR02, Génomique fonctionnelle des tumeurs solides (U674), Institut National de la Santé et de la Recherche Médicale (INSERM), Université de la Méditerranée - Aix-Marseille 2, Physiopathologie des inferctions extra-intestinales à Escherichia coli en pédiatrie, Université Paris Diderot - Paris 7 (UPD7), University of California [San Diego] (UC San Diego), University of California (UC), Department of Molecular Biology, INSERM, Région Ile-de-France, the Broad Medical Research Program, the Association François Aupetit, the Mairie de Paris, the Fondation de la Recherche Medicale, a MESR french fellowship to SEM, the Swedish Research Council, and the National Institutes of Health, University of California, ProdInra, Migration, and May, Robin Charles

Subjects
Infectious Diseases/Gastrointestinal Infections, Nod2 Signaling Adaptor Protein, Yersinia pseudotuberculosis Infections, Apoptosis, Microbiology/Innate Immunity, souris, Inbred C57BL, Transgenic, Mice, Peyer's Patches, 0302 clinical medicine, NOD2, 2.1 Biological and endogenous factors, Yersinia pseudotuberculosis, Homeostasis, Aetiology, 0303 health sciences, Gastrointestinal tract, Multidisciplinary, biology, mus musculus, Foodborne Illness, 3. Good health, Microbiology/Immunity to Infections, Infectious Diseases, medicine.anatomical_structure, Phenotype, Medicine, 030211 gastroenterology & hepatology, Disease Susceptibility, Infection, Research Article, General Science & Technology, Science, Spleen, Bone Marrow Cells, Mice, Transgenic, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Microbiology, Vaccine Related, 03 medical and health sciences, Immune system, intestin, In vivo, Biodefense, oligomérisation de nucléotides 2 (NOD2), medicine, Animals, Genetic Predisposition to Disease, [SDV.BC] Life Sciences [q-bio]/Cellular Biology, 030304 developmental biology, maladie autoimmune, Innate immune system, Gastroenterology and Hepatology/Inflammatory Bowel Disease, Prevention, biology.organism_classification, digestive system diseases, Mice, Inbred C57BL, Emerging Infectious Diseases, Immunology, Digestive Diseases, immunité, Gene Deletion
Abstract

International audience; Nucleotide oligomerisation domain 2 (NOD2) is a component of the innate immunity known to be involved in the homeostasis of Peyer patches (PPs) in mice. However, little is known about its role during gut infection in vivo. Yersinia pseudotuberculosis is an enteropathogen causing gastroenteritis, adenolymphitis and septicaemia which is able to invade its host through PPs. We investigated the role of Nod2 during Y. pseudotuberculosis infection. Death was delayed in Nod2 deleted and Crohn’s disease associated Nod2 mutated mice orogastrically inoculated with Y. pseudotuberculosis. In PPs, the local immune response was characterized by a higher KC level and a more intense infiltration by neutrophils and macrophages. The apoptotic and bacterial cell counts were decreased. Finally, Nod2 deleted mice had a lower systemic bacterial dissemination and less damage of the haematopoeitic organs. This resistance phenotype was lost in case of intraperitoneal infection. We concluded that Nod2 contributes to the susceptibility to Y. pseudotuberculosis in mice.

Published
2008
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