MAVS deficiency induces gut dysbiotic microbiota conferring a proallergic phenotype.

Référence:

Proc Natl Acad Sci U S A. 2018 Sep 24.

Auteurs:

Plantamura E, Dzutsev A, Chamaillard M, Djebali S, Moudombi L, Boucinha L, Grau M, Macari C, Bauché D, Dumitrescu O, Rasigade JP, Lippens S, Plateroti M, Kress E, Cesaro A, Bondu C, Rothermel U, Heikenwälder M, Lina G, Bentaher-Belaaouaj A, Marie JC, Caux C, Trinchieri G, Marvel J, Michallet MC.

Découvrez l’équipe Immunité et Lymphocytes cytotoxiques dirigée par Jacqueline Marvel

Communiqué de presse:

Décryptage du lien entre microbiote intestinal et allergie cutanée

http://www2.cnrs.fr/presse/communique/5696.htm

Résumé:

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.

 

Lien vers l’article:

http://www.pnas.org/content/115/41/10404.long

Affiliations des auteurs :

Plantamura E1, Dzutsev A2,3, Chamaillard M4,5,6,7, Djebali S1, Moudombi L1, Boucinha L1, Grau M1, Macari C1, Bauché D8,9,10, Dumitrescu O1,11, Rasigade JP1,11, Lippens S12, Plateroti M8,9, Kress E8,9, Cesaro A4, Bondu C4, Rothermel U13, Heikenwälder M13, Lina G1,11, Bentaher-Belaaouaj A1, Marie JC8,9,10, Caux C8,9, Trinchieri G2, Marvel J1, Michallet MC14.

  1. Centre International de Recherche en Infectiologie, INSERM U1111-CNRS UMR5308, 69365 Lyon Cedex 07, France.
  2. Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702.
  3. Leidos Biomedical Research, Inc., Frederick, MD 21702.
  4. Center for Infection and Immunity of Lille, Institut Pasteur de Lille, INSERM U1019, F-59000 Lille, France.
  5. Center for Infection and Immunity of Lille, University of Lille, F-59000 Lille, France.
  6. UMR 8204, Centre National de la Recherche Scientifique, F-59000 Lille, France.
  7. U1019, Team 7, Equipe Fondation pour la Recherche Médicale, Institut National de la Santé et de la Recherche Médicale, F-59000 Lille, France.
  8. Centre de Recherche en Cancérologie de Lyon, Centre Léon Bérard, INSERM 1052, CNRS 5286, 69008 Lyon, France.
  9. University of Lyon, Université Claude Bernard Lyon 1, 69008 Lyon, France.
  10. Transforming Growth Factor-b and Immune-Evasion Group, German Cancer Research Center, 69120 Heidelberg, Germany.
  11. Department of Clinical Microbiology, Hospices Civils de Lyon, 69002 Lyon, France.
  12. Inflammation Research Center, Department of Biomedical Molecular Biology, Ghent University, Flanders Institute for Biotechnology, 9000 Ghent, Belgium.
  13. Chronic Inflammation and Cancer, German Cancer Research Center, 69120 Heidelberg, Germany.
  14. Centre International de Recherche en Infectiologie, INSERM U1111-CNRS UMR5308, 69365 Lyon Cedex 07, France; marie-cecile.michallet@lyon.unicancer.fr.

 

 

 

 

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