MAVS deficiency induces gut dysbiotic microbiota conferring a proallergic phenotype.
Fiche publication
Date publication
octobre 2018
Journal
Proceedings of the National Academy of Sciences of the United States of America
Auteurs
Membres identifiés du Cancéropôle Est :
Dr PLATEROTI Michelina
Tous les 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
Lien Pubmed
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 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.
Mots clés
MAVS, RIG-like receptors, allergic skin pathologies, dysbiosis
Référence
Proc Natl Acad Sci U S A. 2018 10 9;115(41):10404-10409