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MAVS deficiency induces gut dysbiotic microbiota conferring a proallergic phenotype

  1. Author:
    Plantamura, Emilie
    Dzutsev, Amiran
    Chamaillard, Mathias
    Djebali, Sophia [ORCID]
    Moudombi, Lyvia
    Boucinha, Lilia
    Grau, Morgan
    Macari, Claire
    Bauché, David
    Dumitrescu, Oana
    Rasigade, Jean-Philippe
    Lippens, Saskia
    Plateroti, Michelina
    Kress, Elsa
    Cesaro, Annabelle
    Bondu, Clovis
    Rothermel, Ulrike
    Heikenwälder, Mathias
    Lina, Gerard
    Bentaher-Belaaouaj, Azzak
    Marie, Julien C
    Caux, Christophe
    Trinchieri, Giorgio
    Marvel, Jacqueline
    Michallet, Marie-Cecile

  2. Author Address

    Centre International de Recherche en Infectiologie, INSERM U1111-CNRS UMR5308, 69365 Lyon Cedex 07, France., Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702., Leidos Biomedical Research, Inc., Frederick, MD 21702., Center for Infection and Immunity of Lille, Institut Pasteur de Lille, INSERM U1019, F-59000 Lille, France., Center for Infection and Immunity of Lille, University of Lille, F-59000 Lille, France., UMR 8204, Centre National de la Recherche Scientifique, F-59000 Lille, France., U1019, Team 7, Equipe Fondation pour la Recherche M 233;dicale, Institut National de la Sant 233; et de la Recherche M 233;dicale, F-59000 Lille, France., Centre de Recherche en Canc 233;rologie de Lyon, Centre L 233;on B 233;rard, INSERM 1052, CNRS 5286, 69008 Lyon, France., University of Lyon, Universit 233; Claude Bernard Lyon 1, 69008 Lyon, France., Transforming Growth Factor-b and Immune-Evasion Group, German Cancer Research Center, 69120 Heidelberg, Germany., Department of Clinical Microbiology, Hospices Civils de Lyon, 69002 Lyon, France., Inflammation Research Center, Department of Biomedical Molecular Biology, Ghent University, Flanders Institute for Biotechnology, 9000 Ghent, Belgium., Chronic Inflammation and Cancer, German Cancer Research Center, 69120 Heidelberg, Germany., Centre International de Recherche en Infectiologie, INSERM U1111-CNRS UMR5308, 69365 Lyon Cedex 07, France; marie-cecile.michallet@lyon.unicancer.fr.,
    1. Year: 2018
    2. Date: Oct 9
    3. Epub Date: 2018 09 24
  2. Journal: Proceedings of the National Academy of Sciences of the United States of America
    1. 115
    2. 41
    3. Pages: 10404-10409
  4. Type of Article: Article
  5. ISSN: 0027-8424
  1. Abstract:

    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.

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  1. Keywords:

External Sources

  1. View Full Text
  2. DOI: 10.1073/pnas.1722372115
  3. PMID: 30249647
  4. View record in Web of Science®
  5. WOS: 000446764200067
  6. PII : 1722372115

Library Notes

  1. Fiscal Year: FY2017-2018
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