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7 results on '"maladie inflammatoire intestinale"'

1. Protectin D1n-3 DPA and resolvin D5n-3 DPA are effectors of intestinal protection

Author

Nathalie Vergnolle, Charles N. Serhan, Delphine Bonnet, Trond Vidar Hansen, Thomas Gobbetti, Céline Deraison, Marius Aursnes, Jesmond Dalli, Laurent Alric, Romain A. Colas, Mauro Perretti, Donata Federici Canova, William Harvey Research Institute, Barts and the London Medical School, Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative, and Pain Medicine, Brigham and Women's Hospital [Boston], Brigham & Women’s Hospital [Boston] (BWH), Harvard Medical School [Boston] (HMS), University of Oslo (UiO), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Pharmacochimie et Biologie pour le Développement (PHARMA-DEV), Institut de Recherche pour le Développement (IRD)-Institut de Chimie de Toulouse (ICT), Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université de Toulouse (UT)-Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT), Institut de Recherche en Santé Digestive (IRSD ), Institut National de la Recherche Agronomique (INRA)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Ecole Nationale Vétérinaire de Toulouse (ENVT), Institut National Polytechnique (Toulouse) (Toulouse INP), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM), MCTRinIA (Project ID: 677542 H2020), William Harvey Research Foundation, National Institutes of Health Grant P01GM095467, Grant ERC-2012-STG_20111109, CHU Toulouse [Toulouse], Institut de Recherche pour le Développement (IRD)-Institut de Chimie de Toulouse (ICT-FR 2599), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Institut de Chimie du CNRS (INC)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Institut de Chimie du CNRS (INC), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Recherche Agronomique (INRA)-Ecole Nationale Vétérinaire de Toulouse (ENVT), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), The William Harvey Research Institute, Barts and The London School of Medicine, Queen Mary University of London (QMUL), Department of Pharmaceutical Chemistry, School of Pharmacy, Department of Internal Medicine and Digestive Diseases, Pole Digestif, Centre Hospitalier Universitaire de Toulouse, 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-Institut de Chimie de Toulouse (ICT-FR 2599), and Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Institut de Chimie du CNRS (INC)-Institut de Recherche pour le Développement (IRD)

Subjects
0301 basic medicine, Neutrophils, [SDV]Life Sciences [q-bio], propriété pharmacologique, Inflammation, Pharmacology, 03 medical and health sciences, chemistry.chemical_compound, Intravital microscopy, medicine, Omega-3 fatty acids, inflammation intestinale, Inflammation resolution, Colitis, Cell adhesion, application thérapeutique, chemistry.chemical_classification, Multidisciplinary, Specialized proresolving mediators, Chemistry, Effector, fungi, Lipid signaling, acide gras oméga 3, medicine.disease, maladie inflammatoire intestinale, 3. Good health, 030104 developmental biology, médiateur lipidique, Immunology, pharmacological activity, medicine.symptom, Resolvin, Polyunsaturated fatty acid
Abstract

The resolution of inflammation is an active process orchestrated by specialized proresolving lipid mediators (SPM) that limit the host response within the affected tissue; failure of effective resolution may lead to tissue injury. Because persistence of inflammatory signals is a main feature of chronic inflammatory conditions, including inflammatory bowel diseases (IBDs), herein we investigate expression and functions of SPM in intestinal inflammation. Targeted liquid chromatography-tandem mass spectrometry-based metabololipidomics was used to identify SPMs from n-3 polyunsaturated fatty acids in human IBD colon biopsies, quantifying a significant up-regulation of the resolvin and protectin pathway compared with normal gut tissue. Systemic treatment with protectin (PD)1n-3 DPA or resolvin (Rv)D5n-3 DPA protected against colitis and intestinal ischemia/reperfusion-induced inflammation in mice. Inhibition of 15-lipoxygenase activity reduced PD1n-3 DPA and augmented intestinal inflammation in experimental colitis. Intravital microscopy of mouse mesenteric venules demonstrated that PD1n-3 DPA and RvD5n-3 DPA decreased the extent of leukocyte adhesion and emigration following ischemia-reperfusion. These data were translated by assessing human neutrophil–endothelial interactions under flow: PD1n-3 DPA and RvD5n-3 DPA reduced cell adhesion onto TNF-α–activated human endothelial monolayers. In conclusion, we propose that innovative therapies based on n-3 DPA-derived mediators could be developed to enable antiinflammatory and tissue protective effects in inflammatory pathologies of the gut.

Published
2017
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2. Netrin-1 up-regulation in inflammatory bowel diseases is required for colorectal cancer progression

Author

Jean-Guy Delcros, Magali Svrcek, Carine Maisse, Nicolas Gadot, Jean-Yves Scoazec, Patrick Mehlen, Jean-François Fléjou, Florian Lepinasse, Clemens Neufert, Marie-May Coissieux, Andrea Paradisi, Céline Delloye-Bourgeois, Apoptose Cancer et Développement, Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS), Université de Lyon, ANIPATH, U865, Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), UMR S 893, Team 13 Microsatellite Instability and Cancers, Medical Clinic, Johannes Gutenberg - Universität Mainz (JGU), Institute for Molecular Medicine, Centre National de la Recherche Scientifique, Centre Leon Berard, Ligue Contre le Cancer, Institut National du Cancer, Agence Nationale de la Recherche, European Union Specific Targeted Research Projects Hermione and APOSYS : Association pour la Recherche contre le Cancer-Institut National du Cancer, and Association pour la Recherche contre le Cancer

Subjects
Colorectal cancer, [SDV]Life Sciences [q-bio], Apoptosis, Disease, souris, 0302 clinical medicine, Netrin, 0303 health sciences, Mice, Inbred BALB C, Multidisciplinary, évolution de la maladie, Caspase 3, NF-kappa B, cell line, Netrin-1, Biological Sciences, Ulcerative colitis, Immunohistochemistry, 3. Good health, Up-Regulation, reverse transcriptase polymerase chain reaction, lignée cellulaire, régulation positive des récepteurs, suppresseur de tumeur, cancer colorectal, 030220 oncology & carcinogenesis, Female, medicine.symptom, Colorectal Neoplasms, HT29 Cells, Signal Transduction, mice, Inflammation, transduction du signal, Mouse model of colorectal and intestinal cancer, 03 medical and health sciences, disease progression, Cell Line, Tumor, medicine, Animals, Humans, rt pcr, Nerve Growth Factors, Autocrine signalling, 030304 developmental biology, apoptose, business.industry, Tumor Suppressor Proteins, Cancer, medicine.disease, HCT116 Cells, Inflammatory Bowel Diseases, maladie inflammatoire intestinale, digestive system diseases, Immunology, Cancer research, business, colorectal neoplasm
Abstract

Chronic inflammation and cancer are intimately associated. This is particularly true for inflammatory bowel diseases (IBD), such as ulcerative colitis and Crohn's disease, which show a major increased risk for colorectal cancer. While the understanding of the molecular pathogenesis of IBD has recently improved, the mechanisms that link these chronic inflammatory states to colorectal cancer development are in large part unknown. One of these mechanisms is NF-κB pathway activation which in turn may contribute to tumor formation by providing anti-apoptotic survival signals to the epithelial cells. Based on the observation that netrin-1, the anti-apoptotic ligand for the dependence receptors DCC and UNC5H is up-regulated in colonic crypts in response to NF-κB, we show here that colorectal cancers from inflammatory bowel diseases patients have selected up-regulation of netrin-1. Moreover, we demonstrate that this inflammation-driven netrin-1 up-regulation is causal for colorectal cancer development as interference with netrin-1 autocrine loop in a mouse model for ulcerative colitis-associated colorectal cancer, while showing no effect on inflammation, inhibits colorectal cancer progression.

Published
2009
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3. Dietary Supplementation with a Low Dose of Polyphenol-Rich Grape Pomace Extract Prevents Dextran Sulfate Sodium-Induced Colitis in Rats

Author

Didier Fraisse, Bruno Pereira, Catherine Felgines, Marie-Paule Vasson, Ahlem Boussenna, Juliette Joubert-Zakeyh, Odile Texier, Unité de Nutrition Humaine (UNH), Université d'Auvergne - Clermont-Ferrand I (UdA)-Clermont Université-Institut National de la Recherche Agronomique (INRA), 3inature Biosphère, Anatomie et cytologie pathologiques, CHU Clermont-Ferrand, Délégation à la Recherche Clinique et à l'Innovation (DRCI), 3inature Biosphere, Institut National de la Recherche Agronomique (INRA)-Université d'Auvergne - Clermont-Ferrand I (UdA)-Clermont Université, Unité de Nutrition Humaine - Clermont Auvergne (UNH), Institut National de la Recherche Agronomique (INRA)-Université Clermont Auvergne (UCA), and Centre Hospitalier Universitaire de Clermont-Ferrand

Subjects
Male, 0301 basic medicine, 040301 veterinary sciences, Anti-Inflammatory Agents, Medicine (miscellaneous), Inflammatory bowel disease, Antioxidants, aliment enrichi, 0403 veterinary science, 03 medical and health sciences, polyphénol, medicine, Animals, grape pomace extract, Vitis, Dietary supplementation, rat, Food science, Rats, Wistar, Colitis, Dextran Sulfate Sodium, Acute colitis, polyphenols, Peroxidase, marc de raisin, 030109 nutrition & dietetics, Nutrition and Dietetics, colon, Plant Extracts, Superoxide Dismutase, Chemistry, Dextran Sulfate, Low dose, fungi, Pomace, food and beverages, 04 agricultural and veterinary sciences, Inflammatory Bowel Diseases, medicine.disease, maladie inflammatoire intestinale, 3. Good health, Polyphenol, inflammation, Fruit, Dietary Supplements, [SDV.AEN]Life Sciences [q-bio]/Food and Nutrition, Phytotherapy, rôle protecteur
Abstract

Evidence from several epidemiological and experimental studies points to a beneficial role of dietary polyphenols in inflammatory bowel disease. In this study, we investigate the protective effect of dietary supplementation with various amounts of a polyphenol-rich grape pomace extract (GPE) on the development of dextran sulfate sodium (DSS)-induced colitis in rats. Rats were fed 21 days on a semisynthetic diet enriched with GPE (0.1%, 0.5%, and 1%), and acute colitis was induced by DSS (40 g/L in the drinking water) administration during the last 7 days. The low GPE content in the diet (0.1%) attenuated clinical signs and colon shortening and limited DSS-induced histological lesions. GPE 0.1% also attenuated the DSS-induced increase in myeloperoxidase activity and improved superoxide dismutase activity. Higher amounts of GPE in the diet induced only weak and nonsignificant protective effects. These results suggest that consumption of a low amount of polyphenol-rich GPE helps protect against colitis development.

Published
2016
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4. Identification of Metabolic Signatures Linked to Anti-Inflammatory Effects of Faecalibacterium prausnitzii

Author

Harry Sokol, Luis G. Bermúdez-Humarán, Chantal Bridonneau, Marion Leclerc, Trent R. Northen, Benjamin P. Bowen, Philippe Langella, Marion Lenoir, Sylvie Miquel, Florian Chain, Rebeca Martín, Sylvie Hudault, Sébastien Raguideau, Muriel Thomas, MICrobiologie de l'ALImentation au Service de la Santé (MICALIS), Institut National de la Recherche Agronomique (INRA)-AgroParisTech, Life Science Division [LBNL Berkeley], Lawrence Berkeley National Laboratory [Berkeley] (LBNL), French group of faecal microbotia transplantation (FGFT), CHU Saint-Antoine [APHP], Université Pierre et Marie Curie - Paris 6 (UPMC), Service de Gastroentérologie, CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Vitagora Competitive Cluster, French FUI (Fond Unique Interministeriel) F1010012D, FEDER (Fonds Europeen de Developpement Regional) 34606, Burgundy Region, Conseil General 21, Grand Dijon, Merck Medication Familiale (Dijon, France), Biovitis (Saint Etienne de Chomeil, France), Langella, Philippe, MICrobiologie de l'ALImentation au Service de la Santé humaine ( MICALIS ), Institut National de la Recherche Agronomique ( INRA ) -AgroParisTech, Life Sciences Division, Lawrence Berkeley National Laboratory, Lawrence Berkeley National Laboratory [Berkeley] ( LBNL ), French group of faecal microbotia transplantation ( FGFT ), Gastroenterology and nutrition department, Université Pierre et Marie Curie - Paris 6 ( UPMC ) -CHU Saint-Antoine [APHP], and Université Pierre et Marie Curie - Paris 6 ( UPMC )

Subjects
Male, Anti-Inflammatory Agents, Firmicutes, Faecalibacterium prausnitzii, Ileum, Biology, medicine.disease_cause, Microbiology, Feces, 03 medical and health sciences, Cecum, In vivo, Virology, medicine, Animals, Intestinal Mucosa, Colitis, Escherichia coli, Acute colitis, 030304 developmental biology, Mice, Inbred BALB C, 0303 health sciences, Gastrointestinal tract, 030306 microbiology, microbiote fécal, [SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, medicine.disease, biology.organism_classification, maladie inflammatoire intestinale, QR1-502, 3. Good health, flore fécale, medicine.anatomical_structure, Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization, colite, Immunology, [ SDV.MHEP.HEG ] Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, Blood Chemical Analysis, Research Article
Abstract

Faecalibacterium prausnitzii is an anti-inflammatory commensal bacterium identified on the basis of human clinical data. The mechanisms underlying its beneficial effects are still unknown. Gnotobiotic mice harboring F. prausnitzii (A2-165) and Escherichia coli (K-12 JM105) were subjected to 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced acute colitis. The inflammatory colitis scores and a gas chromatography-time of flight (GC/TOF) mass spectrometry-based metabolomic profile were monitored in blood, ileum, cecum, colon, and feces in gnotobiotic mice. The potential anti-inflammatory metabolites were tested in vitro. We obtained stable E. coli and F. prausnitzii-diassociated mice in which E. coli primed the gastrointestinal tract (GIT), allowing a durable and stable establishment of F. prausnitzii. The disease activity index, histological scores, myeloperoxidase (MPO) activity, and serum cytokine levels were significantly lower in the presence of F. prausnitzii after TNBS challenge. The protective effect of F. prausnitzii against colitis was correlated to its implantation level and was linked to overrepresented metabolites along the GIT and in serum. Among 983 metabolites in GIT samples and serum, 279 were assigned to known chemical reactions. Some of them, belonging to the ammonia (α-ketoglutarate), osmoprotective (raffinose), and phenolic (including anti-inflammatory shikimic and salicylic acids) pathways, were associated with a protective effect of F. prausnitzii, and the functional link was established in vitro for salicylic acid. We show for the first time that F. prausnitzii is a highly active commensal bacterium involved in reduction of colitis through in vivo modulation of metabolites along the GIT and in the peripheral blood., IMPORTANCE Inflammatory bowel diseases (IBD) are characterized by low proportions of F. prausnitzii in the gut microbiome. This commensal bacterium exhibits anti-inflammatory effects through still unknown mechanisms. Stable monoassociated rodents are actually not a reproducible model to decipher F. prausnitzii protective effects. We propose a new gnotobiotic rodent model providing mechanistic clues. In this model, F. prausnitzii exhibits protective effects against an acute colitis and a protective metabolic profile is linked to its presence along the digestive tract. We identified a molecule, salicylic acid, directly involved in the protective effect of F. prausnitzii. Targeting its metabolic pathways could be an attractive therapeutic strategy in IBD.

Published
2015
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5. Faecalibacterium prausnitzii prevents physiological damages in a chronic low-grade inflammation murine model

Author

Harry Sokol, Philippe Langella, Jennifer Jury, Jun Lu, Florian Chain, Elena F. Verdu, Premysl Bercik, Jane M. Natividad, Rebeca Martín, Sylvie Miquel, Luis G. Bermúdez-Humarán, Vassilia Theodorou, MICrobiologie de l'ALImentation au Service de la Santé humaine ( MICALIS ), Institut National de la Recherche Agronomique ( INRA ) -AgroParisTech, Farncombe Family Digestive Health Research Institute, McMaster University [Hamilton, Ontario], Department of Medical Biochemistry and Biophysics, karolinska institute-Medical Nobel Institute for Biochemistry, Université Pierre et Marie Curie - Paris 6 ( UPMC ), Institut national de la recherche agronomique [Toulouse] ( INRA Toulouse ), Vitagora Competitive Cluster, French FUI (Fond Unique Interministeriel, FUI) [F1010012D], FEDER (Fonds Europeen de Developpement Regional) [Bourgogne: 34606], Burgundy Region, Conseil General 21, Merck Medication Familiale (Dijon, France), Biovitis (Saint Etienne de Chomeil, France), CCFC grants, Grand Dijon, MICrobiologie de l'ALImentation au Service de la Santé (MICALIS), Institut National de la Recherche Agronomique (INRA)-AgroParisTech, CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Laboratoire des biomolécules (LBM UMR 7203), Chimie Moléculaire de Paris Centre (FR 2769), École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Ecole Superieure de Physique et de Chimie Industrielles de la Ville de Paris (ESPCI Paris), Université Paris sciences et lettres (PSL)-Institut de Chimie du CNRS (INC)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Institut de Chimie du CNRS (INC)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Département de Chimie - ENS Paris, Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Neuro-Gastroentérologie & Nutrition (ToxAlim-NGN), ToxAlim (ToxAlim), Institut National de la Recherche Agronomique (INRA)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Ecole Nationale Vétérinaire de Toulouse (ENVT), Institut National Polytechnique (Toulouse) (Toulouse INP), 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)-Institut National de la Recherche Agronomique (INRA)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT), Centre National de la Recherche Scientifique (CNRS)-Sorbonne Université (SU)-Département de Chimie - ENS Paris, École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Chimie Moléculaire de Paris Centre (FR 2769), Institut de Chimie du CNRS (INC)-École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Toulouse III - Paul Sabatier (UT3), 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), 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)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Recherche Agronomique (INRA), Université Pierre et Marie Curie - Paris 6 (UPMC), and Institut National de la Recherche Agronomique (INRA)

Subjects
Microbiology (medical), Serotonin, Colon, medicine.medical_treatment, Faecalibacterium prausnitzii, Inflammation, Biology, Low-grade inflammation, Microbiology, Permeability, law.invention, Enteritis, 03 medical and health sciences, Probiotic, Mice, IBD-remission, 0302 clinical medicine, law, medicine, Animals, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Colitis, [ SDV.BBM ] Life Sciences [q-bio]/Biochemistry, Molecular Biology, 030304 developmental biology, Microbiota, Dysbiosis, Probiotics, 0303 health sciences, Clostridiales, Intestinal permeability, Benzenesulfonates, probiotique, medicine.disease, biology.organism_classification, maladie inflammatoire intestinale, 3. Good health, Disease Models, Animal, Cytokine, microflore digestive, Immunology, Cytokines, 030211 gastroenterology & hepatology, bactérie intestinale, medicine.symptom, Research Article
Abstract

Background The human gut houses one of the most complex and abundant ecosystems composed of up to 1013-1014 microorganisms. The importance of this intestinal microbiota is highlighted when a disruption of the intestinal ecosystem equilibrium appears (a phenomenon called dysbiosis) leading to an illness status, such as inflammatory bowel diseases (IBD). Indeed, the reduction of the commensal bacterium Faecalibacterium prausnitzii (one of the most prevalent intestinal bacterial species in healthy adults) has been correlated with several diseases, including IBD, and most importantly, it has been shown that this bacterium has anti-inflammatory and protective effects in pre-clinical models of colitis. Some dysbiosis disorders are characterized by functional and physiological alterations. Here, we report the beneficial effects of F. prausnitzii in the physiological changes induced by a chronic low-grade inflammation in a murine model. Chronic low-grade inflammation and gut dysfunction were induced in mice by two episodes of dinitro-benzene sulfonic acid (DNBS) instillations. Markers of inflammation, gut permeability, colonic serotonin and cytokine levels were studied. The effects of F. prausnitzii strain A2-165 and its culture supernatant (SN) were then investigated. Results No significant differences were observed in classical inflammation markers confirming that inflammation was subclinical. However, gut permeability, colonic serotonin levels and the colonic levels of the cytokines IL-6, INF-γ, IL-4 and IL-22 were higher in DNBS-treated than in untreated mice. Importantly, mice treated with either F. prausnitzii or its SN exhibited significant decreases in intestinal permeability, tissue cytokines and serotonin levels. Conclusions Our results show that F. prausnitzii and its SN had beneficial effects on intestinal epithelial barrier impairment in a chronic low-grade inflammation model. These observations confirm the potential of this bacterium as a novel probiotic treatment in the management of gut dysfunction and low-grade inflammation. Electronic supplementary material The online version of this article (doi:10.1186/s12866-015-0400-1) contains supplementary material, which is available to authorized users.

Published
2015
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6. CD4CD8αα Lymphocytes, A Novel Human Regulatory T Cell Subset Induced by Colonic Bacteria and Deficient in Patients with Inflammatory Bowel Disease

Author

Guillaume Meurette, Chantal Bridonneau, Nathalie Labarrière, Anne Jarry, Francine Jotereau, Laurence Preisser, Joe-Marc Chauvin, Frédéric Altare, Karim Asehnoune, Guillaume Sarrabayrouse, Harry Sokol, Elodie Quévrain, Céline Bossard, Université de Nantes (UN), University of Pittsburgh School of Medicine, Pennsylvania Commonwealth System of Higher Education (PCSHE), Biomarqueurs prédictifs de la progression des metaplasies et dysplasies des epitheliums (Biométadys), Centre hospitalier universitaire de Nantes (CHU Nantes), Microorganismes, Molécules Bioactives et Physiopathologie Intestinale (LBM-E4), Institut National de la Santé et de la Recherche Médicale (INSERM)-Laboratoire des biomolécules (LBM UMR 7203), Chimie Moléculaire de Paris Centre (FR 2769), École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Ecole Superieure de Physique et de Chimie Industrielles de la Ville de Paris (ESPCI Paris), Université Paris sciences et lettres (PSL)-Institut de Chimie du CNRS (INC)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Institut de Chimie du CNRS (INC)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Département de Chimie - ENS Paris, Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Chimie Moléculaire de Paris Centre (FR 2769), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), MICrobiologie de l'ALImentation au Service de la Santé (MICALIS), AgroParisTech-Université Paris-Saclay-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Université d'Angers (UA), Thérapeutiques cliniques et expérimentales des infections (EA 3826) (EA 3826), Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN), Jarry, Anne, Centre de Recherche en Cancérologie Nantes-Angers (CRCNA), Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM)-PRES Université Nantes Angers Le Mans (UNAM)-Hôtel-Dieu de Nantes-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hôpital Laennec-Centre National de la Recherche Scientifique (CNRS)-Faculté de Médecine d'Angers-Centre hospitalier universitaire de Nantes (CHU Nantes), Neuropathies du système nerveux entérique et pathologies digestives, implication des cellules gliales entériques, Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM), Inflammation intestinale, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Recherche Agronomique (INRA)-AgroParisTech, CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), The work was supported by grants from FP7, ANR and Cancéropôle Grand Ouest 2009. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript., Centre de Recherche en Cancérologie / Nantes - Angers (CRCNA), CHU Saint-Antoine [APHP], Bernardo, Elizabeth, Centre National de la Recherche Scientifique (CNRS)-Sorbonne Université (SU)-Département de Chimie - ENS Paris, École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Chimie Moléculaire de Paris Centre (FR 2769), Institut de Chimie du CNRS (INC)-École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Sorbonne Université (SU)-Département de Chimie - ENS Paris, and Université Paris sciences et lettres (PSL)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
[SDV.IMM] Life Sciences [q-bio]/Immunology, Regulatory T cell, QH301-705.5, [SDV]Life Sciences [q-bio], réponse immunitaire, Faecalibacterium prausnitzii, cytométrie de flux, chemical and pharmacologic phenomena, Biology, Gut flora, lymphocyte, Inflammatory bowel disease, digestive system, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, 0302 clinical medicine, Immune system, Intestinal mucosa, lymphocyte t, medicine, Biology (General), 030304 developmental biology, 0303 health sciences, General Immunology and Microbiology, General Neuroscience, FOXP3, hemic and immune systems, medicine.disease, biology.organism_classification, maladie inflammatoire intestinale, 3. Good health, [SDV] Life Sciences [q-bio], régulateur de réponse, medicine.anatomical_structure, 030220 oncology & carcinogenesis, Immunology, monocyte, [SDV.IMM]Life Sciences [q-bio]/Immunology, clostridium, General Agricultural and Biological Sciences, Dysbiosis
Abstract

How the microbiota affects health and disease is a crucial question. In mice, gut Clostridium bacteria are potent inducers of colonic interleukin (IL)-10-producing Foxp3 regulatory T cells (Treg), which play key roles in the prevention of colitis and in systemic immunity. In humans, although gut microbiota dysbiosis is associated with immune disorders, the underlying mechanism remains unknown. In contrast with mice, the contribution of Foxp3 Treg in colitis prevention has been questioned, suggesting that other compensatory regulatory cells or mechanisms may exist. Here we addressed the regulatory role of the CD4CD8 T cells whose presence had been reported in the intestinal mucosa and blood. Using colonic lamina propria lymphocytes (LPL) and peripheral blood lymphocytes (PBL) from healthy individuals, and those with colon cancer and irritable bowel disease (IBD), we demonstrated that CD4CD8 (DP8) T lymphocytes expressed most of the regulatory markers and functions of Foxp3 Treg and secreted IL-10. Strikingly, DP8 LPL and PBL exhibited a highly skewed repertoire toward the recognition of Faecalibacterium prausnitzii, a major Clostridium species of the human gut microbiota, which is decreased in patients with IBD. Furthermore, the frequencies of DP8 PBL and colonic LPL were lower in patients with IBD than in healthy donors and in the healthy mucosa of patients with colon cancer, respectively. Moreover, PBL and LPL from most patients with active IBD failed to respond to F. prausnitzii in contrast to PBL and LPL from patients in remission and/or healthy donors. These data (i) uncover a Clostridium-specific IL-10-secreting Treg subset present in the human colonic LP and blood, (ii) identify F. prausnitzii as a major inducer of these Treg, (iii) argue that these cells contribute to the control or prevention of colitis, opening new diagnostic and therapeutic strategies for IBD, and (iv) provide new tools to address the systemic impact of both these Treg and the intestinal microbiota on the human immune homeostasis. Author Summary It has become evident that bacteria in our gut affect health and disease, but less is known about how they do this. Recent studies in mice showed that gut Clostridium bacteria and their metabolites can activate regulatory T cells (Treg) that in turn mediate tolerance to signals that would ordinarily cause inflammation. In this study we identify a subset of human T lymphocytes, designated CD4CD8 T cells that are present in the surface lining of the colon and in the blood. We demonstrate Treg activity and show these cells to be activated by microbiota; we identify F. prausnitzii, a core Clostridium strain of the human gut microbiota, as a major inducer of these Treg cells. Interestingly, there are fewer F. prausnitzii in individuals suffering from inflammatory bowel disease (IBD), and accordingly the CD4CD8 T cells are decreased in the blood and gut of patients with IBD. We argue that CD4CD8 colonic Treg probably help control or prevent IBD. These data open the road to new diagnostic and therapeutic strategies for the management of IBD and provide new tools to address the impact of the intestinal microbiota on the human immune system.

Published
2014
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7. Deoxynivalenol as a new factor in the persistence of intestinal inflammatory diseases: An emerging hypothesis through possible modulation of Th17-mediated response

Author

Roberta Abrami, Laurence Guzylack-Piriou, François Meurens, Patricia M. Cano, Isabelle P. Oswald, Juliette Cognie, Julie Seeboth, Toxicologie Alimentaire (UTA), Institut National de la Recherche Agronomique (INRA)-Université de Bourgogne (UB)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement, UR Infectiologie animale et Santé publique (UR IASP), Institut National de la Recherche Agronomique (INRA), Vaccine and Infectious Disease Organization, University of Saskatchewan [Saskatoon] (U of S), Physiologie de la reproduction et des comportements [Nouzilly] (PRC), Centre National de la Recherche Scientifique (CNRS)-Université de Tours-Institut Français du Cheval et de l'Equitation [Saumur]-Institut National de la Recherche Agronomique (INRA), INRA, ANSES (France), Ministry for Education and Research (France), CAPES-COFECUB (Brazil), INRA-Division of animal health, ToxAlim (ToxAlim), Université Toulouse III - Paul Sabatier (UT3), 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), Infectiologie et Santé Publique (UMR ISP), Institut National de la Recherche Agronomique (INRA)-Université de Tours, Institut National de la Recherche Agronomique (INRA)-Institut Français du Cheval et de l'Equitation [Saumur]-Université de Tours-Centre National de la Recherche Scientifique (CNRS), State University of Londrina = Universidade Estadual de Londrina, Biosynthèse & Toxicité des Mycotoxines (ToxAlim-BioToMyc), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Recherche Agronomique (INRA)-Université Toulouse III - Paul Sabatier (UT3), Oswald, Isabelle, Guzylack-Piriou, Laurence, Institut National de la Recherche Agronomique (INRA)-Université de Tours (UT), Institut National de la Recherche Agronomique (INRA)-Institut Français du Cheval et de l'Equitation [Saumur]-Université de Tours (UT)-Centre National de la Recherche Scientifique (CNRS), Toxicologie Alimentaire ( UTA ), Institut National de la Recherche Agronomique ( INRA ) -Université de Bourgogne ( UB ) -AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement, UR Infectiologie animale et Santé publique ( UR IASP ), Institut National de la Recherche Agronomique ( INRA ), University of Saskatchewan [Saskatoon] ( U of S ), Physiologie de la reproduction et des comportements [Nouzilly] ( PRC ), and Institut National de la Recherche Agronomique ( INRA ) -Institut Français du Cheval et de l'Equitation [Saumur]-Université de Tours-Centre National de la Recherche Scientifique ( CNRS )

Subjects
Chemokine, Anatomy and Physiology, système immunitaire, Sus scrofa, Digestive Physiology, Veterinary Toxicology, deoxynivalenol, lcsh:Medicine, Toxicology, T-Lymphocytes, Regulatory, Persistence (computer science), Immune tolerance, chemistry.chemical_compound, Immunotoxicology, Immune Physiology, Intestinal Mucosa, lcsh:Science, Immune Response, 0303 health sciences, Multidisciplinary, T Cells, santé animale, 030302 biochemistry & molecular biology, food and beverages, rt pcr quantitative, 3. Good health, Inflammatory mediator, Intestines, Jejunum, Veterinary Diseases, Veterinary Mycology, Models, Animal, Cytokines, medicine.symptom, Chemokines, Inflammation Mediators, Research Article, Autre (Sciences du Vivant), [SDV.OT]Life Sciences [q-bio]/Other [q-bio.OT], analyse protéomique, mycotoxine, Immune Cells, Animal Types, Immunology, Toxic Agents, Inflammation, Immunopathology, Biology, In Vitro Techniques, Large Animals, Cell Line, Immunomodulation, 03 medical and health sciences, arn, Immune system, medicine, Animals, RNA, Messenger, [ SDV.OT ] Life Sciences [q-bio]/Other [q-bio.OT], Mycotoxin, 030304 developmental biology, Gene Expression Profiling, lcsh:R, Dendritic Cells, maladie inflammatoire intestinale, étude transcriptomique, chemistry, Gene Expression Regulation, santé publique, biology.protein, Th17 Cells, Digestive tract, Veterinary Science, lcsh:Q, Trichothecenes, Digestive System
Abstract

Background/Aims: Deoxynivalenol (DON) is a mycotoxin produced by Fusarium species which is commonly found in temperate regions worldwide as a natural contaminant of cereals. It is of great concern not only in terms of economic losses but also in terms of animal and public health. The digestive tract is the first and main target of this food contaminant and it represents a major site of immune tolerance. A finely tuned cross-talk between the innate and the adaptive immune systems ensures the homeostatic equilibrium between the mucosal immune system and commensal microorganisms. The aim of this study was to analyze the impact of DON on the intestinal immune response. Methodology: Non-transformed intestinal porcine epithelial cells IPEC-1 and porcine jejunal explants were used to investigate the effect of DON on the intestinal immune response and the modulation of naive T cells differentiation. Transcriptomic proteomic and flow cytometry analysis were performed. Results: DON induced a pro-inflammatory response with a significant increase of expression of mRNA encoding for IL-8, IL-1 alpha and IL-1 beta, TNF-alpha in all used models. Additionally, DON significantly induced the expression of genes involved in the differentiation of Th17 cells (STAT3, IL-17A, IL-6, IL-1 beta) at the expenses of the pathway of regulatory T cells (Treg) (FoxP3, RALDH1). DON also induced genes related to the pathogenic Th17 cells subset such as IL-23A, IL-22 and IL-21 and not genes related to the regulatory Th17 cells (rTh17) such as TGF-beta and IL-10. Conclusion: DON triggered multiple immune modulatory effects which could be associated with an increased susceptibility to intestinal inflammatory diseases.

Published
2013
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