MAVS deficiency induces gut dysbiotic microbiota conferring a proallergic phenotype - Centre de recherche en cancérologie de Lyon (UMR INSERM 1052 ; CNRS 5286 ; Centre Léon Bérard) Accéder directement au contenu
Article Dans Une Revue Proceedings of the National Academy of Sciences of the United States of America Année : 2018

MAVS deficiency induces gut dysbiotic microbiota conferring a proallergic phenotype

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.

Dates et versions

hal-02398995 , version 1 (08-12-2019)

Identifiants

Citer

Emilie Plantamura, Amiran Dzutsev, Mathias Chamaillard, Sophia Djebali, Lyvia Moudombi, et al.. MAVS deficiency induces gut dysbiotic microbiota conferring a proallergic phenotype. Proceedings of the National Academy of Sciences of the United States of America, 2018, 115 (41), pp.10404-10409. ⟨10.1073/pnas.1722372115⟩. ⟨hal-02398995⟩
116 Consultations
0 Téléchargements

Altmetric

Partager

Gmail Facebook X LinkedIn More