MAVS deficiency induces gut dysbiotic microbiota conferring a proallergic phenotype

Autor: Elsa Kress, Mathias Heikenwalder, Gerard Lina, David Bauché, Saskia Lippens, Claire Macari, Marie-Cécile Michallet, Mathias Chamaillard, Sophia Djebali, Emilie Plantamura, Lyvia Moudombi, Jacqueline Marvel, Christophe Caux, Julien C. Marie, Annabelle Cesaro, Lilia Boucinha, Amiran Dzutsev, Jean-Philippe Rasigade, Ulrike Rothermel, Giorgio Trinchieri, Azzak Bentaher-Belaaouaj, Oana Dumitrescu, Morgan Grau, Michelina Plateroti, Clovis Bondu
Přispěvatelé: Immunité et lymphocytes cytotoxiques – Immunity and cytotoxic lymphocytes, Centre International de Recherche en Infectiologie (CIRI), École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Cancer Inflammation Program [Frederick], Center for Cancer Research, Leidos Biomedical Research, Inc [Frederick, MD, USA], Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 (CIIL), Institut Pasteur de Lille, 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), Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), German Cancer Research Center - Deutsches Krebsforschungszentrum [Heidelberg] (DKFZ), Hospices Civils de Lyon (HCL), Pathogénie des Staphylocoques – Staphylococcal Pathogenesis (StaPath), VIB-UGent Center for Inflammation Research [Gand, Belgique] (IRC), VIB [Belgium], We acknowledge the contributions of the Structure Fédérative de Recherche BioSciences Gerland-Lyon Sud (UMS3444/US8-Ecole Normale Superieure de Lyon, Universite Claude Bernard de Lyon CNRS, INSERM) facilities, especially AniRA ImmOS. This work was supported by Institut National de la Santé et de la Recherche Médicale, Centre National de la Recherche Scientifique, Université de Lyon I, Hospices Civils de Lyon, Association 'ARCHE,' and Agence Nationale de la Recherche Grant ANR-11-RPIB-0019-03 (to J.M.), a grant from the Département du Rhône-Fonds Européen de Développement Régional (PLATINE) (J.M.), and European Commission Grant LSHG-CT-2006-037188, The European Mouse Disease Clinic (to J.M.)., We thank J. Tschopp’s laboratory for Cardif (MAVS-deficient) mice, Martine Tomkowiak, Julien Mafille, and Barbara Gilbert for expert technical assistance, Anca Hennino for confocal images, Christophe Arpin and Mohamad Sobh for statistical data analysis, Bertrand Dubois, Marc Vocanson, and Jean-François Nicolas for helpful discussions on the DTH model, Thierry Walzer, Laurent Genestier, Bertrand Dubois, and Gérard Eberl for critical reading of the manuscript, Bariza Blanquier for help with qPCR analysis (genetic analysis), Thibault Andrieu and Sébastien Dussurgey (AniRA-Cytometry), Olga Azocar and Christophe Chamot from the Plateau Technique Imagerie/Microcopie, and the staff of AniRA-PBES, especially Jean-Louis Thoumas and Céline Angleraux., Centre International de Recherche en Infectiologie - UMR (CIRI), École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), 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), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), MICHALLET, MARIE-CECILE
Jazyk: angličtina
Rok vydání: 2018
Předmět:
0301 basic medicine
MESH: Signal Transduction
RIG-like receptors
MESH: Intestines/immunology
MESH: Skin Diseases
Bacterial/pathology
Gut flora
MESH: Skin Diseases
Bacterial/metabolism
MESH: Mice
Knockout
[SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunity
Mice
0302 clinical medicine
MESH: Animals
MESH: Hypersensitivity/metabolism
[SDV.IMM.ALL]Life Sciences [q-bio]/Immunology/Allergology
Sensitization
Mice
Knockout
Multidisciplinary
integumentary system
dysbiosis
Biological Sciences
MAVS
Phenotype
3. Good health
Intestines
medicine.anatomical_structure
MESH: Intestines/pathology
030220 oncology & carcinogenesis
[SDV.IMM]Life Sciences [q-bio]/Immunology
Female
[SDV.IMM.ALL] Life Sciences [q-bio]/Immunology/Allergology
Signal Transduction
MESH: Intestines/microbiology
[SDV.IMM] Life Sciences [q-bio]/Immunology
MESH: Dysbiosis/complications
Biology
MESH: Gastrointestinal Microbiome/immunology
MESH: Phenotype
digestive system
03 medical and health sciences
MESH: Skin Diseases
Bacterial/etiology
MESH: Hypersensitivity/etiology
Immunity
MESH: Mice
Inbred C57BL
MESH: Homeodomain Proteins/metabolism
medicine
Hypersensitivity
allergic skin pathologies
MESH: Hypersensitivity/pathology
Animals
Colitis
Allergic contact dermatitis
[SDV.IMM.II] Life Sciences [q-bio]/Immunology/Innate immunity
MESH: Mice
Adaptor Proteins
Signal Transducing
Homeodomain Proteins
MESH: Adaptor Proteins
Signal Transducing/physiology
Intestinal permeability
Skin Diseases
Bacterial
medicine.disease
biology.organism_classification
Gastrointestinal Microbiome
Mice
Inbred C57BL
Disease Models
Animal
030104 developmental biology
Immunology
MESH: Homeodomain Proteins/genetics
MESH: Disease Models
Animal
Dysbiosis
MESH: Female
Zdroj: Proceedings of the National Academy of Sciences of the United States of America
Proceedings of the National Academy of Sciences of the United States of America, 2018, 115 (41), pp.10404-10409. ⟨10.1073/pnas.1722372115⟩
Proceedings of the National Academy of Sciences of the United States of America, National Academy of Sciences, 2018, 115 (41), pp.10404-10409. ⟨10.1073/pnas.1722372115⟩
ISSN: 0027-8424
1091-6490
DOI: 10.1073/pnas.1722372115⟩
Popis: International audience; Prominent changes in the gut microbiota (referred to as "dysbiosis") play a key role in the development of allergic disorders, but the underlying mechanisms remain unknown. Study of the delayed-type hypersensitivity (DTH) response in mice contributed to our knowledge of the pathophysiology of human allergic contact dermatitis. Here we report a negative regulatory role of the RIG-I-like receptor adaptor mitochondrial antiviral signaling (MAVS) on DTH by modulating gut bacterial ecology. Cohousing and fecal transplantation experiments revealed that the dysbiotic microbiota of Mavs -/- mice conferred a proallergic phenotype that is communicable to wild-type mice. DTH sensitization coincided with increased intestinal permeability and bacterial translocation within lymphoid organs that enhanced DTH severity. Collectively, we unveiled an unexpected impact of RIG-I-like signaling on the gut microbiota with consequences on allergic skin disease outcome. Primarily, these data indicate that manipulating the gut microbiota may help in the development of therapeutic strategies for the treatment of human allergic skin pathologies.
Databáze: OpenAIRE
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