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1. In vivo commensal control of Clostridioides difficile virulence

Author

Mario L. Arrieta-Ortiz, Johann Peltier, Andrew B. Onderdonk, Selva Rupa Christinal Immanuel, Narjol Gonzalez-Escalona, Nicholas DiBenedetto, Richard Lavin, Nitin S. Baliga, Marc W. Allard, Maria Hoffman, Abraham L. Sonenshein, Yan Luo, Christopher K Cummins, Brintha P. Girinathan, Lynn Bry, Bruno Dupuy, Jay N. Worley, Mary L. Delaney, Georg K. Gerber, Brigham & Women’s Hospital [Boston] (BWH), Harvard Medical School [Boston] (HMS), National Center for Biotechnology Information (NCBI), Pathogénèse des Bactéries Anaérobies / Pathogenesis of Bacterial Anaerobes (PBA (U-Pasteur_6)), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Institut de Biologie Intégrative de la Cellule (I2BC), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS), Institute for Systems Biology [Seattle] (ISB), U.S. Food and Drug Administration (FDA), Harvard-MIT Division of Health Sciences and Technology [Cambridge], Massachusetts Institute of Technology (MIT), Tufts University School of Medicine [Boston], This work was supported by the BWH Precision Medicine Institute, R01AI153605 from the National Institute of Allergy and Infectious Diseases (NIAID) and P30DK034854 from the National Institute of Diabetes, Digestive and Kidney Diseases to L.B., R01AI128215, R01AI141953, and U19AI135976 from NIAID and IIBR-2042948 from the National Science Foundation to N.S.B., B.P.G. was supported by T32 HL007627, and the work of J.N.W. was supported by the Intramural Research Program of the National Library of Medicine, National Institutes of Health. J.P. received support from the Institut Pasteur (Bourse ROUX). This work was conducted by authors from the FDA working as official U.S. Government employees and for which no additional external funding was utilized.

Subjects
MESH: Clostridioides difficile, MESH: Amino Acids, colitis, Systems biology, MESH: Clostridium Infections, [SDV]Life Sciences [q-bio], gnotobiotic mouse, Clostridium sardiniense, Virulence, MESH: Butyrates, Biology, MESH: Virulence, medicine.disease_cause, Microbiology, MESH: Clostridiales, MESH: Fermentation, Clostridia, MESH: Gene Expression Profiling, conventional mouse, In vivo, Virology, MESH: Germ-Free Life, MESH: Severity of Illness Index, medicine, Paraclostridium bifermentans, MESH: Animals, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Colitis, Pathogen, MESH: Mice, MESH: Gene Regulatory Networks, MESH: Gene Expression Regulation, Bacterial, metatranscriptomics, MESH: Symbiosis, Toxin, Host (biology), Clostridioides difficile, MESH: Clostridium, MESH: Arginine, MESH: Cecum, biology.organism_classification, medicine.disease, metabolomics, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, MESH: Systems Biology, Parasitology, carbon source enrichment analysis, anaerobe metabolism
Abstract

International audience; Leveraging systems biology approaches, we illustrate how metabolically distinct species of Clostridia protect against or worsen Clostridioides difficile infection in mice by modulating the pathogen's colonization, growth, and virulence to impact host survival. Gnotobiotic mice colonized with the amino acid fermenter Paraclostridium bifermentans survive infection with reduced disease severity, while mice colonized with the butyrate-producer, Clostridium sardiniense, succumb more rapidly. Systematic in vivo analyses revealed how each commensal alters the gut-nutrient environment to modulate the pathogen's metabolism, gene regulatory networks, and toxin production. Oral administration of P. bifermentans rescues conventional, clindamycin-treated mice from lethal C. difficile infection in a manner similar to that of monocolonized animals, thereby supporting the therapeutic potential of this commensal species. Our findings lay the foundation for mechanistically informed therapies to counter C. difficile disease using systems biology approaches to define host-commensal-pathogen interactions in vivo.

Published
2021

2. If Channel Inhibition With Ivabradine Does Not Improve Cardiac and Vascular Function in Experimental Septic Shock

Author

Huguette Louis, Narimane Al Kattani, Antoine Kimmoun, Eliane Albuisson, Bruno Levy, Chaojie Wei, Défaillance Cardiovasculaire Aiguë et Chronique (DCAC), Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lorraine (UL), ESPRI-Biobase [CHRU Nancy] (Unité fonctionnelle de la plateforme d’aide à la recherche clinique), Institut Élie Cartan de Lorraine (IECL), Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS), Service de Réanimation Médicale [CHRU Nancy], and Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)

Subjects
Male, MESH: Interleukin-10, Hemodynamics, 030204 cardiovascular system & hematology, Critical Care and Intensive Care Medicine, 0302 clinical medicine, Heart Rate, Ivabradine, MESH: Animals, MESH: Heart Rate, Cecum, Shock, Septic, 3. Good health, Interleukin-10, Echocardiography, Shock (circulatory), Anesthesia, Emergency Medicine, Cardiology, Tumor necrosis factor alpha, MESH: Benzazepines, medicine.symptom, MESH: Cardiovascular Agents, medicine.drug, medicine.medical_specialty, MESH: Hemodynamics, MESH: Rats, MESH: Shock, Septic, Proinflammatory cytokine, 03 medical and health sciences, [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, Internal medicine, Heart rate, medicine, Animals, Rats, Wistar, Ligation, business.industry, Septic shock, Interleukin-6, Tumor Necrosis Factor-alpha, 030208 emergency & critical care medicine, Cardiovascular Agents, MESH: Cecum, MESH: Rats, Wistar, Benzazepines, MESH: Ligation, medicine.disease, MESH: Interleukin-6, MESH: Male, Rats, MESH: Tumor Necrosis Factor-alpha, Cardiovascular agent, MESH: Echocardiography, business
Abstract

International audience; OBJECTIVE:Previous studies have suggested that lowering heart rate (HR) by selective β1-blockers improves sepsis-induced cardiac and vascular dysfunction primarily by decreasing proinflammatory pathways. However, the impact of isolated heart rate reduction (HRR) on hemodynamics and inflammatory pathways remains unknown. The present study was designed to assess the effects of HRR by ivabradine, an If channel inhibitor, on cardiovascular function and inflammatory pathways in peritonitis-induced septic shock in rats.DESIGN:Randomized animal study.SETTING:University research laboratory.INTERVENTIONS:Four hours after cecal ligation and puncture (CLP), Wistar rats were randomly allocated to the following groups: CLP (n = 8) and CLP + ivabradine (n = 8, administered per os 4 h after the surgery). Another eight Wistar male rats underwent sham operation. All rats received a continuous infusion of saline (10 mL kg h), analgesic (nalbuphine: 0.2 mg kg h), and antibiotics (imipenem and cilastatin sodium: 10 mg kg) 4 h after the surgery. Assessment at 18 h included hemodynamics, in vivo cardiac function by echocardiography, and ex vivo vasoreactivity by myography. Circulating cytokine levels (TNF-α, IL-6, and IL-10) were measured by ELISA, whereas cardiac and vascular protein expressions of NF-κB/IκBα/iNOS and Akt/eNOS were assessed by Western blotting.RESULTS:Compared with sham animals, CLP induced tachycardia, hypotension, decreased cardiac output, hyperlactatemia, and vascular hyporesponsiveness to vasopressors. Compared with the CLP group, adjunction of ivabradine decreased the HR without any impact on blood pressure, lactatemia, or vascular responsiveness to vasopressors. Adjunction of ivabradine to CLP rats had no impact on TNF-α, IL-6, and IL-10 cytokines, or on the protein expression levels of phosphorylated forms of NF-κB, Akt, eNOS, and degradation of IκBα in cardiac and vascular tissues.CONCLUSION:Isolated HRR by ivabradine in an experimental model of septic shock does not appear to be associated with any effect on the tested parameters of cardiac function or on vascular responsiveness to vasopressors. Moreover, in this setting, ivabradine does not alter the circulating levels of selected pro/anti-inflammatory cytokines or cardiac and vascular NF-κB/IκBα protein expression levels.

Published
2016

3. Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fat Diet–Induced Obesity and Diabetes in Mice

Author

Rémy Burcelin, Claude Knauf, Nathalie M. Delzenne, Rodrigo Bibiloni, Audrey M. Neyrinck, Patrice D. Cani, Aurélie Waget, Simon, Marie Francoise, Unit of Pharmacokinetics, Metabolism, Nutrition, and Toxicology (PMNT-73/69), Université Catholique de Louvain = Catholic University of Louvain (UCL), Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Nutrition and Health, Nestlé Research Center | Centre de recherche Nestlé [Lausanne], Nestlé S.A.-Nestlé S.A., Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), and Nestlé Research Center

Subjects
Male, MESH: Inflammation, MESH: Bifidobacterium, Lipopolysaccharide, Endocrinology, Diabetes and Metabolism, Mice, Obese, Adipose tissue, Type 2 diabetes, MESH: Bacteroides, MESH: Base Sequence, Gut flora, medicine.disease_cause, MESH: Genotype, Feces, Mice, chemistry.chemical_compound, 0302 clinical medicine, MESH: Reverse Transcriptase Polymerase Chain Reaction, MESH: Diabetes Mellitus, Experimental, Bacteroides, MESH: Obesity, MESH: Animals, Cecum, MESH: Mice, Obese, 2. Zero hunger, 0303 health sciences, Reverse Transcriptase Polymerase Chain Reaction, MESH: Feces, MESH: Crosses, Genetic, Anti-Bacterial Agents, 3. Good health, RNA, Bacterial, Female, medicine.symptom, MESH: RNA, Bacterial, medicine.medical_specialty, Genotype, 030209 endocrinology & metabolism, Inflammation, Biology, digestive system, Diabetes Mellitus, Experimental, 03 medical and health sciences, MESH: Mice, Inbred C57BL, MESH: Anti-Bacterial Agents, Internal medicine, Diabetes mellitus, Internal Medicine, medicine, Animals, Obesity, MESH: Mice, Crosses, Genetic, 030304 developmental biology, Intestinal permeability, Base Sequence, MESH: Cecum, medicine.disease, biology.organism_classification, Endotoxemia, MESH: Male, Mice, Inbred C57BL, Lactobacillus, Endocrinology, chemistry, MESH: Endotoxemia, Immunology, Bifidobacterium, MESH: Female, MESH: Lactobacillus, Oxidative stress
Abstract

OBJECTIVE—Diabetes and obesity are characterized by a low-grade inflammation whose molecular origin is unknown. We previously determined, first, that metabolic endotoxemia controls the inflammatory tone, body weight gain, and diabetes, and second, that high-fat feeding modulates gut microbiota and the plasma concentration of lipopolysaccharide (LPS), i.e., metabolic endotoxemia. Therefore, it remained to demonstrate whether changes in gut microbiota control the occurrence of metabolic diseases. RESEARCH DESIGN AND METHODS—We changed gut microbiota by means of antibiotic treatment to demonstrate, first, that changes in gut microbiota could be responsible for the control of metabolic endotoxemia, the low-grade inflammation, obesity, and type 2 diabetes and, second, to provide some mechanisms responsible for such effect. RESULTS—We found that changes of gut microbiota induced by an antibiotic treatment reduced metabolic endotoxemia and the cecal content of LPS in both high-fat–fed and ob/ob mice. This effect was correlated with reduced glucose intolerance, body weight gain, fat mass development, lower inflammation, oxidative stress, and macrophage infiltration marker mRNA expression in visceral adipose tissue. Importantly, high-fat feeding strongly increased intestinal permeability and reduced the expression of genes coding for proteins of the tight junctions. Furthermore, the absence of CD14 in ob/ob CD14−/− mutant mice mimicked the metabolic and inflammatory effects of antibiotics. CONCLUSIONS—This new finding demonstrates that changes in gut microbiota controls metabolic endotoxemia, inflammation, and associated disorders by a mechanism that could increase intestinal permeability. It would thus be useful to develop strategies for changing gut microbiota to control, intestinal permeability, metabolic endotoxemia, and associated disorders.

Published
2008

4. Adaptive strategies and pathogenesis of Clostridium difficile from in vivo transcriptomics

Author

Laxmee Caleechum, Anne Collignon, Frédéric Barbut, Sylvie Bouttier, Marc Monot, Fátima C. Pereira, Cécile Denève, Claire Janoir, Sandra Hoys, Bruno Dupuy, Adriano O. Henriques, Diana Chapeton-Montes, EA 4043, Université Paris-Sud - Paris 11 (UP11), CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Pathogénèse des Bactéries Anaérobies / Pathogenesis of Bacterial Anaerobes (PBA (U-Pasteur_6)), Institut Pasteur [Paris]-Université Paris Diderot - Paris 7 (UPD7), Bactéries anaérobies et Toxines, Institut Pasteur [Paris], Instituto de Tecnologia Química e Biológica António Xavier (ITQB), Universidade Nova de Lisboa = NOVA University Lisbon (NOVA), Service de Microbiologie [Hôpital Jean Verdier], Hôpital Jean Verdier [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), This work was funded by the European Community's Seventh Framework Programme HYPERDIFF (grant HEALTH-F3-2008-223585), the Institut Pasteur, the Université Paris-Sud, and the Fundação para a Ciência e a Tecnologia (FCT) (grant Pest-C/EQB/LA0006/2011). C.D. and D.C.-M. were supported by doctoral fellowships from the French Ministry of Higher Education and Research, and F.P. was the recipient of a fellowship from the FCT (grant SFRH/BD/45459/08)., European Project: 223585,EC:FP7:HEALTH,FP7-HEALTH-2007-B,HYPERDIFF(2008), Institut Pasteur [Paris] (IP)-Université Paris Diderot - Paris 7 (UPD7), Institut Pasteur [Paris] (IP), National reference laboratory for clostridium difficile, Université Pierre et Marie Curie - Paris 6 (UPMC)-AP-HP - Hôpital Saint-Antoine, Universidade Nova de Lisboa (NOVA), Hôpital Jean Verdier [Bondy], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP), Bactéries, Pathogènes et Santé (UBaPS), Faculté de Pharmacie, Université Paris-Sud - Paris 11 (UP11)-Université Paris-Sud - Paris 11 (UP11), and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)

Subjects
[SDV]Life Sciences [q-bio], MESH: Virulence, MESH: Genome, Bacterial, Transcriptome, Mice, MESH: Up-Regulation, MESH: Animals, MESH: Stress, Physiological, Cecum, MESH: Bacterial Proteins, Regulation of gene expression, 0303 health sciences, MESH: Gene Expression Regulation, Bacterial, Virulence, MESH: Peptidoglycan, Clostridium difficile, Adaptation, Physiological, Up-Regulation, Infectious Diseases, Host adaptation, MESH: Mutation, Virulence Factors, MESH: Clostridium Infections, Immunology, Peptidoglycan, Biology, Microbiology, 03 medical and health sciences, Bacterial Proteins, In vivo, Stress, Physiological, Animals, Author Correction, Gene, MESH: Mice, MESH: Clostridium difficile, 030304 developmental biology, MESH: Virulence Factors, Microarray analysis techniques, 030306 microbiology, Clostridioides difficile, MESH: Cecum, [SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, Gene Expression Regulation, Bacterial, Molecular Pathogenesis, MESH: Adaptation, Physiological, Mutation, Clostridium Infections, Parasitology, Genome, Bacterial
Abstract

Clostridium difficile is currently the major cause of nosocomial intestinal diseases associated with antibiotic therapy in adults. In order to improve our knowledge of C. difficile -host interactions, we analyzed the genome-wide temporal expression of C. difficile 630 genes during the first 38 h of mouse colonization to identify genes whose expression is modulated in vivo , suggesting that they may play a role in facilitating the colonization process. In the ceca of the C. difficile -monoassociated mice, 549 genes of the C. difficile genome were differentially expressed compared to their expression during in vitro growth, and they were distributed in several functional categories. Overall, our results emphasize the roles of genes involved in host adaptation. Colonization results in a metabolic shift, with genes responsible for the fermentation as well as several other metabolic pathways being regulated inversely to those involved in carbon metabolism. In addition, several genes involved in stress responses, such as ferrous iron uptake or the response to oxidative stress, were regulated in vivo . Interestingly, many genes encoding conserved hypothetical proteins (CHP) were highly and specifically upregulated in vivo . Moreover, genes for all stages of sporulation were quickly induced in vivo , highlighting the observation that sporulation is central to the persistence of C. difficile in the gut and to its ability to spread in the environment. Finally, we inactivated two genes that were differentially expressed in vivo and evaluated the relative colonization fitness of the wild-type and mutant strains in coinfection experiments. We identified a CHP as a putative colonization factor, supporting the suggestion that the in vivo transcriptomic approach can unravel new C. difficile virulence genes.

Published
2013

5. Metabolic adaptation to a high-fat diet is associated with a change in the gut microbiota

Author

Claire Cenac, Pierre Monsan, Aurélie Waget, Pascale Klopp, Philippe Valet, Jacques Amar, Jason S. Iacovoni, Jérôme Mariette, Rémy Burcelin, Mathieu Bergé, Jérôme Lluch, Audrey Baylac, Anne Bouloumié, Sandra Grès, Christophe Klopp, Françoise Ouarné, Christine Roques, Olivier Bouchez, Vassilia Theodorou, Matteo Serino, Elodie Luche, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), 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), Adhésion Bacterienne et Formation de Biofilms, PRES Université de Toulouse, ToxAlim (ToxAlim), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Ecole Nationale Vétérinaire de Toulouse (ENVT), Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Ecole d'Ingénieurs de Purpan (INPT - EI Purpan), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Recherche Agronomique (INRA), Plateforme Bio-informatique Toulouse Genopole®, UBIA INRA, Toulouse Genopole, Génopole Toulouse Midi-Pyrénées [Auzeville] (GENOTOUL), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Ecole Nationale Vétérinaire de Toulouse (ENVT), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Institut National de la Recherche Agronomique (INRA), CRITT Bio-Industrie, Ecole d'Ingénieurs de Purpan (INPT - EI Purpan), Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Recherche Agronomique (INRA)-Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA), Laboratoire d'Ingénierie des Systèmes Biologiques et des Procédés (LISBP), Centre National de la Recherche Scientifique (CNRS)-Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Service de Médecine Interne et Hypertension Artérielle [Toulouse], CHU Toulouse [Toulouse]-Hôpital de Rangueil, CHU Toulouse [Toulouse], his work was supported by grants from Agence Nationale pour la Recherche (ANR) to RB and collaborators (ANR-Florinflam and Transflora), in part, by the European Commission's Seventh Framework programme under grant agreement No 241913 (FLORINASH) to RB and by the Benjamin Delessert Foundation to MS., European Project: 241913,EC:FP7:HEALTH,FP7-HEALTH-2009-single-stage,FLORINASH(2010), Centre National de la Recherche Scientifique - CNRS (FRANCE), Ecole d'Ingénieurs de Purpan - EIP (FRANCE), Institut National Polytechnique de Toulouse - Toulouse INP (FRANCE), Institut National de la Recherche Agronomique - INRA (FRANCE), Institut National des Sciences Appliquées de Toulouse - INSA (FRANCE), Institut National de la Santé et de la Recherche Médicale - INSERM (FRANCE), Institut universitaire de France - IUF (FRANCE), Université Toulouse III - Paul Sabatier - UT3 (FRANCE), Centre Hospitalier Universitaire de Toulouse - CHU Toulouse (FRANCE), ToxAlim (Toulouse, France), Laboratoire d'Ingénierie des Systèmes Biologiques et des Procédés - LISBP (Toulouse, France), Institut National Polytechnique de Toulouse - INPT (FRANCE), Institut National de la Recherche Agronomique (INRA)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Ecole d'Ingénieurs de Purpan (INPT - EI Purpan), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, Institut National de la Recherche Agronomique (INRA)-Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Fédérale Toulouse Midi-Pyrénées, Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Centre National de la Recherche Scientifique (CNRS), Neuro-Gastroentérologie & Nutrition (ToxAlim-NGN), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Recherche Agronomique (INRA)-Université Toulouse III - Paul Sabatier (UT3), Burcelin, Remy, Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Toulouse (UT)-Université de Toulouse (UT)-Ecole Nationale Vétérinaire de Toulouse (ENVT), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université de Toulouse (UT)-Ecole d'Ingénieurs de Purpan (INP - PURPAN), Université de Toulouse (UT)-Université de Toulouse (UT), Unité de Biométrie et Intelligence Artificielle (ancêtre de MIAT) (UBIA), Institut National de la Recherche Agronomique (INRA), Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT), Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Centre National de la Recherche Scientifique (CNRS), Service d'hypertension artérielle et thérapeutique [CHU Toulouse] (HTA et thérapeutique), Pôle Cardiovasculaire et Métabolique [CHU Toulouse], Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Recherche Agronomique (INRA)-Université Toulouse III - Paul Sabatier (UT3), Simon, Marie Francoise, The role of intestinal microflora in non-alcoholic fatty liver disease (NAFLD) - FLORINASH - - EC:FP7:HEALTH2010-01-01 - 2014-12-31 - 241913 - VALID, Institut National des Sciences Appliquées (INSA)-Université Fédérale Toulouse Midi-Pyrénées-Institut National des Sciences Appliquées (INSA)-Université Fédérale Toulouse Midi-Pyrénées-Université Toulouse III - Paul Sabatier (UT3), and Institut National des Sciences Appliquées (INSA)-Université Fédérale Toulouse Midi-Pyrénées-Institut National des Sciences Appliquées (INSA)-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)

Subjects
Lipopolysaccharides, Male, mictobiota, White adipose tissue, [SDV.GEN] Life Sciences [q-bio]/Genetics, Gut flora, Fatty Acids, Nonesterified, Intestinal absorption, Cecum, Mice, 0302 clinical medicine, gut, metabolic, background, phenotype, diet, MESH: Diabetes Mellitus, Experimental, MESH: Animals, 2. Zero hunger, 0303 health sciences, Glucose tolerance test, MESH: Muscle, Skeletal, MESH: Cytokines, MESH: Fatty Acids, Nonesterified, medicine.diagnostic_test, biology, digestive, oral, and skin physiology, Gastroenterology, food and beverages, Phenotype, Adaptation, Physiological, Intestines, medicine.anatomical_structure, High-fat diet, Liver, 030220 oncology & carcinogenesis, MESH: Permeability, Cytokines, medicine.symptom, MESH: Intestines, medicine.medical_specialty, MESH: Glucose Tolerance Test, MESH: Intestinal Absorption, Médecine humaine et pathologie, Inflammation, Gut microbiota, Diet, High-Fat, MESH: Phenotype, digestive system, Permeability, Diabetes Mellitus, Experimental, 03 medical and health sciences, MESH: Mice, Inbred C57BL, Diabetes mellitus, Internal medicine, medicine, Animals, Muscle, Skeletal, MESH: Mice, 030304 developmental biology, [SDV.GEN]Life Sciences [q-bio]/Genetics, Metabolic diseases, MESH: Cecum, Glucose Tolerance Test, MESH: Metagenome, medicine.disease, biology.organism_classification, MESH: Adaptation, Physiological, MESH: Male, Mice, Inbred C57BL, MESH: Diet, High-Fat, Endocrinology, Intestinal Absorption, Immunology, Metagenome, MESH: Lipopolysaccharides, MESH: Liver
Abstract

Chantier qualité GA; International audience; OBJECTIVE: The gut microbiota, which is considered a causal factor in metabolic diseases as shown best in animals, is under the dual influence of the host genome and nutritional environment. This study investigated whether the gut microbiota per se, aside from changes in genetic background and diet, could sign different metabolic phenotypes in mice. METHODS: The unique animal model of metabolic adaptation was used, whereby C57Bl/6 male mice fed a high-fat carbohydrate-free diet (HFD) became either diabetic (HFD diabetic, HFD-D) or resisted diabetes (HFD diabetes-resistant, HFD-DR). Pyrosequencing of the gut microbiota was carried out to profile the gut microbial community of different metabolic phenotypes. Inflammation, gut permeability, features of white adipose tissue, liver and skeletal muscle were studied. Furthermore, to modify the gut microbiota directly, an additional group of mice was given a gluco-oligosaccharide (GOS)-supplemented HFD (HFD+GOS). RESULTS: Despite the mice having the same genetic background and nutritional status, a gut microbial profile specific to each metabolic phenotype was identified. The HFD-D gut microbial profile was associated with increased gut permeability linked to increased endotoxaemia and to a dramatic increase in cell number in the stroma vascular fraction from visceral white adipose tissue. Most of the physiological characteristics of the HFD-fed mice were modulated when gut microbiota was intentionally modified by GOS dietary fibres. CONCLUSIONS: The gut microbiota is a signature of the metabolic phenotypes independent of differences in host genetic background and diet.

Published
2012

6. IL-17A/F-signaling does not contribute to the initial phase of mucosal inflammation triggered by S. Typhimurium

Author

Laurye Van Maele, Jean-Claude Sirard, Till A. Röhn, Manfred Kopf, Pascal Songhet, Delphine Cayet, Manja Barthel, Wolf-Dietrich Hardt, Martin F. Bachmann, Eidgenössische Technische Hochschule - Swiss Federal Institute of Technology [Zürich] (ETH Zürich), Cytos Biotechnology, Cytos Biotechnology, AG, Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 (CIIL), Centre National de la Recherche Scientifique (CNRS)-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Université de Lille-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP), Institute of Integrative Biology, Molecular Biomedicine, Grants to WDH from the Swiss National Science Foundation (310000-113623/1 and 310030-132997/1), the KTI (to MB andWDH) and a grant to JCS and WDH from the European Union (SavinMucoPath INCO-CT-2006-032296)., Sirard, Jean-Claude, Institut Pasteur de Lille, and Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Male, Salmonella typhimurium, MESH: Signal Transduction, Chemokine, Time Factors, medicine.medical_treatment, MESH: Interleukin-17, MESH: Receptors, Interleukin-17, MESH: Mice, Knockout, MESH: Enterocolitis, Type three secretion system, Infectious Diseases/Bacterial Infections, Mice, 0302 clinical medicine, Intestinal mucosa, MESH: Reverse Transcriptase Polymerase Chain Reaction, MESH: Animals, Cecum, Mice, Knockout, 0303 health sciences, MESH: Cytokines, Multidisciplinary, Receptors, Interleukin-17, biology, Effector, Reverse Transcriptase Polymerase Chain Reaction, Interleukin-17, Vaccination, MESH: Chemokines, 3. Good health, CXCL1, Cytokine, Cytokines, Medicine, [SDV.IMM]Life Sciences [q-bio]/Immunology, Female, Interleukin 17, medicine.symptom, Chemokines, Signal Transduction, Research Article, MESH: Mutation, MESH: Salmonella Infections, Animal, [SDV.IMM] Life Sciences [q-bio]/Immunology, Science, Inflammation, Microbiology, 03 medical and health sciences, MESH: Gene Expression Profiling, MESH: Mice, Inbred C57BL, Immunology/Immunity to Infections, medicine, Animals, MESH: Mice, 030304 developmental biology, Salmonella Infections, Animal, Enterocolitis, Gene Expression Profiling, MESH: Time Factors, MESH: Cecum, MESH: Salmonella typhimurium, MESH: Vaccination, MESH: Male, Mice, Inbred C57BL, Immunology, Mutation, Immunology/Immune Response, biology.protein, MESH: Female, 030215 immunology
Abstract

International audience; Salmonella enterica subspecies 1 serovar Typhimurium (S. Typhimurium) causes diarrhea and acute inflammation of the intestinal mucosa. The pro-inflammatory cytokines IL-17A and IL-17F are strongly induced in the infected mucosa but their contribution in driving the tissue inflammation is not understood. We have used the streptomycin mouse model to analyze the role of IL-17A and IL-17F and their cognate receptor IL-17RA in S. Typhimurium enterocolitis. Neutralization of IL-17A and IL-17F did not affect mucosal inflammation triggered by infection or spread of S. Typhimurium to systemic sites by 48 h p.i. Similarly, Il17ra(-/-) mice did not display any reduction in infection or inflammation by 12 h p.i. The same results were obtained using S. Typhimurium variants infecting via the TTSS1 type III secretion system, the TTSS1 effector SipA or the TTSS1 effector SopE. Moreover, the expression pattern of 45 genes encoding chemokines/cytokines (including CXCL1, CXCL2, IL-17A, IL-17F, IL-1α, IL-1β, IFNγ, CXCL-10, CXCL-9, IL-6, CCL3, CCL4) and antibacterial molecules was not affected by Il17ra deficiency by 12 h p.i. Thus, in spite of the strong increase in Il17a/Il17f mRNA in the infected mucosa, IL-17RA signaling seems to be dispensable for eliciting the acute disease. Future work will have to address whether this is attributable to redundancy in the cytokine signaling network.

Published
2010

7. Broilers do not play a dominant role in the Campylobacter fetus contamination of humans

Author

Isabelle Kempf, Valérie Prouzet-Mauléon, Francis Mégraud, Fabienne Dufour-Gesbert, Gwenaëlle Hellard, Laboratoire d'études et de recherches avicoles, porcines et piscicoles, Agence Française de Sécurité Sanitaire des Aliments (AFSSA), Laboratoire de Bactériologie (INSERM ERI10), Université Bordeaux Segalen - Bordeaux 2-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Bordeaux Segalen - Bordeaux 2, Service de virologie et d'immunologie biologique, and CHU Bordeaux [Bordeaux]-Groupe hospitalier Pellegrin

Subjects
Microbiology (medical), medicine.disease_cause, Microbiology, Campylobacter jejuni, Feces, Campylobacter fetus, MESH: Campylobacter Infections, Campylobacter Infections, medicine, Animals, Humans, MESH: Animals, MESH: Food Microbiology, Cecum, Disease Reservoirs, Fetus, MESH: Disease Reservoirs, MESH: Humans, biology, Inoculation, Campylobacter, Campylobacteraceae, MESH: Chickens, MESH: Feces, MESH: Cecum, General Medicine, Contamination, biology.organism_classification, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, Specific Pathogen-Free Organisms, Intestines, MESH: Specific Pathogen-Free Organisms, embryonic structures, Food Microbiology, MESH: Campylobacter fetus, Chickens, Bacteria, MESH: Intestines
Abstract

Campylobacter fetus causes severe infections in humans and can be isolated from various mammals and reptiles. However, although poultry are considered to be the main reservoir of Campylobacter jejuni, little is known about the presence of C. fetus in poultry. Thus, specific pathogen-free chickens were experimentally inoculated with a mixture of either three non-thermotolerant or four thermotolerant human strains of C. fetus. Faecal samples were regularly sampled after inoculation and caeca and intestines were collected 21 or 40 days after inoculation. All samples were analysed for the presence of Campylobacter using culture techniques. No Campylobacter could be re-isolated. This result strongly suggests that broilers do not play an important part in the C. fetus contamination of humans.

Published
2006

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