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1. Pseudomonas fluorescens Alters the Intestinal Barrier Function by Modulating IL-1β Expression Through Hematopoietic NOD2 Signaling

Author

Monique Dussaillant, Maryline Roy, Frédérick Barreau, Nathalie Connil, Kelly Biaggini, Marc G. J. Feuilloley, Nicolas Montcuquet, Ziad Alnabhani, Abdelhak Jallane, Eric Ogier-Denis, Amar Madi, Jean-Pierre Hugot, Interactions hôte-greffon-tumeur, ingénierie cellulaire et génique - UFC (UMR INSERM 1098) (HOTE GREFFON), Université de Franche-Comté (UFC)-Etablissement français du sang [Bourgogne-France-Comté] (EFS [Bourgogne-France-Comté])-Institut National de la Santé et de la Recherche Médicale (INSERM), Biodiversité et Biotechnologie Fongiques (BBF), École Centrale de Marseille (ECM)-Aix Marseille Université (AMU)-Institut National de la Recherche Agronomique (INRA), 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), Faculté de Médecine Xavier Bichat, Laboratoire de Microbiologie du Froid – Signaux et Micro-Environnement (LMDF-SME), Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU), Institut de Recherche pour le Développement, UR 178 Fundamentals & Domains of Disease Emergence (IRD UR178), Laboratoire de Microbiologie Signaux et Microenvironnement (LMSM), Centre de Physiopathologie Toulouse Purpan (CPTP - U1043 INSERM - UMR5282 CNRS - UT3), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Interactions hôte-greffon-tumeur, ingénierie cellulaire et génique - UFC (UMR INSERM 1098) (RIGHT), Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Institut National de la Recherche Agronomique (INRA)-Aix Marseille Université (AMU)-École Centrale de Marseille (ECM), Centre de Physiopathologie Toulouse Purpan (CPTP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS BFC)-Université de Franche-Comté (UFC), Université de Toulouse (UT)-Université de Toulouse (UT)-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)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté]), and Aix Marseille Université (AMU)-Institut National de la Recherche Agronomique (INRA)-École Centrale de Marseille (ECM)

Subjects
Cell Membrane Permeability, Blotting, Western, Interleukin-1beta, Nod2 Signaling Adaptor Protein, Pseudomonas fluorescens, Real-Time Polymerase Chain Reaction, digestive system, Microbiology, Mice, chemistry.chemical_compound, Intestinal mucosa, NOD2, [SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB], Animals, Humans, Immunology and Allergy, Secretion, RNA, Messenger, Intestinal Mucosa, Cells, Cultured, ComputingMilieux_MISCELLANEOUS, Barrier function, Mice, Knockout, biology, Reverse Transcriptase Polymerase Chain Reaction, Chemistry, Macrophages, Gastroenterology, Receptors, Interleukin-1, [SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, Hematopoietic Stem Cells, biology.organism_classification, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, digestive system diseases, Mice, Inbred C57BL, Caco-2, Paracellular transport, Caco-2 Cells, Muramyl dipeptide, Signal Transduction
Abstract

Background Ileal Crohn's disease is related to NOD2 mutations and to a gut barrier dysfunction. Pseudomonas fluorescens has also been associated with ileal Crohn's disease. The aim of this study was to determine the impact of P. fluorescens on the paracellular permeability in ileum and Peyer's patches. Methods To explore this question, in vivo and ex vivo experiments were performed in wild-type, Nod2, Nod2, and IL-1R mice together with in vitro analyses using the Caco-2 (epithelial) and the THP-1 (monocyte) human cell lines. Results Pseudomonas fluorescens increased the paracellular permeability of the intestinal mucosa through the secretion of IL-1β by the immune cell populations and the activation of myosin light chain kinase in the epithelial cells. Induction of the IL-1β pathway required the expression of Nod2 in the hematopoietic compartment, and muramyl dipeptide (a Nod2 ligand) had an inhibitory effect. Conclusions Pseudomonas fluorescens thus alters the homeostasis of the epithelial barrier function by a mechanism similar to that previously observed for Yersinia pseudotuberculosis. This work further documents a putative role of psychrotrophic bacteria in Crohn's disease.

Published
2015
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2. The horse pinworm (Oxyuris equi) in archaeology during the Holocene: Review of past records and new data

Author

Sébastien Lepetz, Jean-Pierre Hugot, Benjamin Dufour, Matthieu Le Bailly, Laboratoire Chrono-environnement ( LCE ), Université Bourgogne Franche-Comté ( UBFC ) -Centre National de la Recherche Scientifique ( CNRS ) -Université de Franche-Comté ( UFC ), UMR 843 Inflammation intestinale pathologique de l'enfant, Institut National de la Santé et de la Recherche Médicale, Archéozoologie, archéobotanique : sociétés, pratiques et environnements ( AASPE ), Centre National de la Recherche Scientifique ( CNRS ) -Muséum National d'Histoire Naturelle ( MNHN ), Laboratoire Chrono-environnement - CNRS - UBFC (UMR 6249) (LCE), Centre National de la Recherche Scientifique (CNRS)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Institut National de la Santé et de la Recherche Médicale (INSERM), Archéozoologie, archéobotanique : sociétés, pratiques et environnements (AASPE), and Muséum national d'Histoire naturelle (MNHN)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Microbiology (medical), [ SDV.MP.PAR ] Life Sciences [q-bio]/Microbiology and Parasitology/Parasitology, Old World, Paleoparasitology, Central asia, Enterobiasis, Biology, Before Present, Microbiology, Archaeology, Oxyuris equi, Infectious Diseases, Western europe, Genetics, Period (geology), Animals, [SDV.MP.PAR]Life Sciences [q-bio]/Microbiology and Parasitology/Parasitology, Horse Diseases, Enterobius, Horses, Molecular Biology, Ecology, Evolution, Behavior and Systematics, Holocene, ComputingMilieux_MISCELLANEOUS
Abstract

This paper focuses on the horse pinworm, Oxyuris equi, in archaeology during the Holocene period, and presents an overview of past published occurrences, early mentions in texts, and new data from our paleoparasitology research. This original compilation shows that the most ancient record of the horse pinworm dates to ca. 2500 years before present (ybp) in Central Asia and to ca. 2020 ybp in Western Europe. It also shows that the parasite is not detected on the American continent until contemporary periods. The role of European migrations from 1492 (Christopher Columbus) is discussed to explain the transfer of the horse pinworm from the Old World to the Americas. The absence of any record of this parasite before ca. 2500 ybp in Eurasia could be explained by parasite ecology, unfavorable sampling and scarcity of horse archeological remains. For the Americas, the absence of horse for long periods can be an additional explanation for the absence of the parasite.

Published
2015
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3. Titanium dioxide nanoparticle impact and translocation through ex vivo, in vivo and in vitro gut epithelia

Author

Barbara Fayard, Christine Carapito, Emilie Brun, Aloïse Mabondzo, Marie Carrière, S. Sorieul, Frédérick Barreau, Giulia Veronesi, Thierry Rabilloud, Nathalie Herlin-Boime, Corinne Chanéac, BMC, Ed., Service Interdisciplinaire sur les Systèmes Moléculaires et les Matériaux (ex SCM) (SIS2M UMR 3299), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), Inflammation intestinale pathologique de l'enfant, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Physiopathologie Toulouse Purpan (CPTP), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), European Synchrotron Radiation Facility (ESRF), Centre d'Etudes Nucléaires de Bordeaux Gradignan (CENBG), Université Sciences et Technologies - Bordeaux 1 (UB)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Chimie de la Matière Condensée de Paris (LCMCP), Université Pierre et Marie Curie - Paris 6 (UPMC)-Collège de France (CdF (institution))-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Spectrométrie de Masse BioOrganique [Strasbourg] (LSMBO), Département Sciences Analytiques et Interactions Ioniques et Biomoléculaires (DSA-IPHC), Institut Pluridisciplinaire Hubert Curien (IPHC), Université de Strasbourg (UNISTRA)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS)-Institut Pluridisciplinaire Hubert Curien (IPHC), Université de Strasbourg (UNISTRA)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Chimie et Biologie des Métaux (LCBM - UMR 5249), Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Institut de Recherche Interdisciplinaire de Grenoble (IRIG), Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Institut de Biologie et de Technologies de Saclay (IBITECS), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay, Laboratoire Francis PERRIN (LFP - URA 2453), Institut Nanosciences et Cryogénie (INAC), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019]), This work was funded by the region Ile de France through the framework C'nano Ile de France (NanoDIG project), by INERIS in the context of the post-Grenelle program (NANOTRANS project) and was partly performed in the context of Labex SERENADE., Université Sciences et Technologies - Bordeaux 1-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS), Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS)-Institut Pluridisciplinaire Hubert Curien (IPHC), Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS), Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche Interdisciplinaire de Grenoble (IRIG), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Grenoble Alpes [2016-2019] (UGA [2016-2019]), Université Paris-Saclay-Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS)-Institut de Chimie du CNRS (INC), Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Collège de France (CdF (institution))-Institut de Chimie du CNRS (INC), Université Grenoble Alpes [2016-2019] (UGA [2016-2019])-Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université de Strasbourg (UNISTRA)-Université de Haute-Alsace (UHA) Mulhouse - Colmar (Université de Haute-Alsace (UHA))-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Université de Haute-Alsace (UHA) Mulhouse - Colmar (Université de Haute-Alsace (UHA))-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS)-Institut Pluridisciplinaire Hubert Curien (IPHC), and Université de Strasbourg (UNISTRA)-Université de Haute-Alsace (UHA) Mulhouse - Colmar (Université de Haute-Alsace (UHA))-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Université de Haute-Alsace (UHA) Mulhouse - Colmar (Université de Haute-Alsace (UHA))-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Pathology, medicine.medical_specialty, Materials science, Cell Survival, Health, Toxicology and Mutagenesis, Translocation, Ileum, Toxicology, Real-Time Polymerase Chain Reaction, digestive system, Paracellular, Intestinal absorption, Epithelium, Cell Line, Mice, Nanoparticle, Microscopy, Electron, Transmission, Suspensions, Accumulation, M-cells, medicine, Animals, Humans, Gut, Microfold cell, Titanium, Tight junction, Toxicity, Research, Ingestion, digestive, oral, and skin physiology, technology, industry, and agriculture, Spectrometry, X-Ray Emission, Biological Transport, General Medicine, Cell biology, Gut Epithelium, Gastrointestinal Tract, medicine.anatomical_structure, X-Ray Absorption Spectroscopy, Intestinal Absorption, [SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie, Paracellular transport, Nanoparticles, Titanium dioxide, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, Ex vivo, Dissolution
Abstract

International audience; BACKGROUND: TiO2 particles are commonly used as dietary supplements and may contain up to 36% of nano-sized particles (TiO2-NPs). Still impact and translocation of NPs through the gut epithelium is poorly documented. RESULTS: We show that, in vivo and ex vivo, agglomerates of TiO2-NPs cross both the regular ileum epithelium and the follicle-associated epithelium (FAE) and alter the paracellular permeability of the ileum and colon epithelia. In vitro, they accumulate in M-cells and mucus-secreting cells, much less in enterocytes. They do not cause overt cytotoxicity or apoptosis. They translocate through a model of FAE only, but induce tight junctions remodeling in the regular ileum epithelium, which is a sign of integrity alteration and suggests paracellular passage of NPs. Finally we prove that TiO2-NPs do not dissolve when sequestered up to 24 h in gut cells. CONCLUSIONS: Taken together these data prove that TiO2-NPs would possibly translocate through both the regular epithelium lining the ileum and through Peyer's patches, would induce epithelium impairment, and would persist in gut cells where they would possibly induce chronic damage.

Published
2014
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4. 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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5. 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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6. 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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7. 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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8. 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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9. Perspectives on Applied Spatial Analysis to Animal Health: a Case of Rodents in Thailand

Author

Herbreteau, Vincent, Demoraes, Florent, Hugot, Jean-Pierre, Pattamaporn, K., Salem, Gérard, Souris, Marc, Gonzalez, Jean-Paul, Institut des Sciences de l'Evolution de Montpellier (UMR ISEM), Centre de Coopération Internationale en Recherche Agronomique pour le Développement (Cirad)-École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université de Montpellier (UM)-Institut de recherche pour le développement [IRD] : UR226-Centre National de la Recherche Scientifique (CNRS), Institut de Recherche pour le Développement, UR 178 Fundamentals & Domains of Disease Emergence (IRD UR178), Pharmacogénétique et abords thérapeutiques des maladies héréditaires, Institut National de la Santé et de la Recherche Médicale (INSERM), Fondation Jean Dausset, Inflammation intestinale pathologique de l'enfant, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Center of Excellence for Vectors and Vector-Borne Diseases (CVVD), Mahidol University [Bangkok], Laboratoire Espace, Santé et Territoire (LEST), Université Paris Nanterre (UPN), Conditions et territoires d'émergence des maladies : dynamiques spatio-temporelles de l'émergence, évolution, diffusion/réduction des maladies, résistance et prémunition des hôtes (CTEM), Centre de Coopération Internationale en Recherche Agronomique pour le Développement (Cirad)-École pratique des hautes études (EPHE), and Demoraes, Florent

Subjects
geographic information systems, spatial analysis, NDVI, ANALYSE SPATIALE, [SHS.GEO] Humanities and Social Sciences/Geography, [SHS.GEO]Humanities and Social Sciences/Geography, Bandicoot, RONGEUR, ASTER, [SDE.BE] Environmental Sciences/Biodiversity and Ecology, remote sensing, SAVI, savilei, POPULATION ANIMALE, rodents, SANTE, Bandicota, [SDE.BE]Environmental Sciences/Biodiversity and Ecology, ComputingMilieux_MISCELLANEOUS, biogeography, Bandicota indica
Abstract

International audience

Published
2006
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10. Use of geographic information system and remote sensing for assessing environment influence on leptospirosis incidence, Phrae province, Thailand

Author

Vincent Herbreteau, Florent Demoraes, Wasana Khaungaew, Jean-Pierre Hugot, Jean-Paul Gonzalez, Pattamaporn Kittayapong, Marc Souris, Institut des Sciences de l'Evolution de Montpellier (UMR ISEM), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université de Montpellier (UM)-Centre de Coopération Internationale en Recherche Agronomique pour le Développement (Cirad)-Centre National de la Recherche Scientifique (CNRS)-Institut de recherche pour le développement [IRD] : UR226, Institut de Recherche pour le Développement, UR 178 Fundamentals & Domains of Disease Emergence (IRD UR178), Phrae provincial Public Health Office, Ministry of Public Health - Thailande, Pharmacogénétique et abords thérapeutiques des maladies héréditaires, Institut National de la Santé et de la Recherche Médicale (INSERM), Fondation Jean Dausset, Inflammation intestinale pathologique de l'enfant, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Conditions et territoires d'émergence des maladies : dynamiques spatio-temporelles de l'émergence, évolution, diffusion/réduction des maladies, résistance et prémunition des hôtes (CTEM), Center of Excellence for Vectors and Vector-Borne Diseases (CVVD), Mahidol University [Bangkok], Centre de Coopération Internationale en Recherche Agronomique pour le Développement (Cirad)-École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université de Montpellier (UM)-Institut de recherche pour le développement [IRD] : UR226-Centre National de la Recherche Scientifique (CNRS), Centre de Coopération Internationale en Recherche Agronomique pour le Développement (Cirad)-École pratique des hautes études (EPHE), and Demoraes, Florent

Subjects
Rice growing, EPIDEMIOLOGIE, SYSTEME D'INFORMATION GEOGRAPHIQUE, Epidemiology, [SHS.GEO] Humanities and Social Sciences/Geography, Geographic Information System, TELEDETECTION SPATIALE, POPULATION RURALE, [SHS.GEO]Humanities and Social Sciences/Geography, Remote sensing, Environment, Rodents, RIZICULTURE, PREVALENCE, RONGEUR, Exposure, INFECTION, Prevalence, GESTION DE L'ENVIRONNEMENT, RESERVOIR, Leptospirosis, Infection, LEPTOSPIROSE
Abstract

International audience; Severe epidemics of leptospirosis yearly occurred in Thailand since 1997, causing over 1,200 deaths, especially among farmers highly exposed while working in flooded rice fields. Main vectors are wild rodents, spreading the human pathogenic bacteria (spirocheta) in the environment through their urine. Phrae province, which has recorded among the highest incidences, was chosen for a large scale spatial analysis, in collaboration with Phrae provincial Public Health Office. A health geographic database (GIS) was built, using SavGIS, a Geographic Information System (GIS) and Remote Sensing (RS) freeware developed by the Development Research French Institute (IRD), to understand the disease dynamics and assess the villagers' exposure. GIS and Remote Sensing processing have shown a great potential in analyzing vector-borne diseases but have never been applied to leptospirosis. The land use was extracted and vegetation indices computed from a TERRA ASTER satellite image and described around villages. In a second step, this information was compared with the reported disease incidence. Problems encountered due to the accuracy of biomedical and location-based data are detailed. The results are exposed and discussed in a preventive planning perspective.

Published
2006

11. Yersinia pseudotuberculosis infection disrupts the intestinal barrier and enables systemic translocation of Yersinia and bacteria from the gut flora in mice

Author

Ulrich Meinzer, Frederick Barreau, Sophie Esmiol-Welterlin, Camille Jung, Dominique Berrebi, Monique Dussaillant, Stéphane Bonacorsi, Hans Wolfwatz, Julie Perroy, Vincent Ollendorff, Jean-Pierre Hugot, ProdInra, Migration, Inflammation intestinale pathologique de l'enfant, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), AP-HP Hôpital universitaire Robert-Debré [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Université Paris 1 Panthéon-Sorbonne (UP1), AP-HP Hôpital Bicêtre (Le Kremlin-Bicêtre), Dynamique Musculaire et Métabolisme (DMEM), Institut National de la Recherche Agronomique (INRA)-Université de Montpellier (UM), Université Montpellier 2 - Sciences et Techniques (UM2), Université Paris Diderot - Paris 7 (UPD7), Department of Molecular Biology, Umeå University, Institut de Génomique Fonctionnelle (IGF), and 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)

Subjects
[SDV] Life Sciences [q-bio], [SDV]Life Sciences [q-bio], yersinia pseudotuberculosis, [INFO]Computer Science [cs], [INFO] Computer Science [cs], ComputingMilieux_MISCELLANEOUS
Abstract

International audience

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