Fiche publication
Date publication
mars 2020
Journal
Cell reports
Auteurs
Membres identifiés du Cancéropôle Est :
Dr FRISCH Benoit
Tous les auteurs :
Sencio V, Barthelemy A, Tavares LP, Machado MG, Soulard D, Cuinat C, Queiroz-Junior CM, Noordine ML, Salomé-Desnoulez S, Deryuter L, Foligné B, Wahl C, Frisch B, Vieira AT, Paget C, Milligan G, Ulven T, Wolowczuk I, Faveeuw C, Le Goffic R, Thomas M, Ferreira S, Teixeira MM, Trottein F
Lien Pubmed
Résumé
Secondary bacterial infections often complicate viral respiratory infections. We hypothesize that perturbation of the gut microbiota during influenza A virus (IAV) infection might favor respiratory bacterial superinfection. Sublethal infection with influenza transiently alters the composition and fermentative activity of the gut microbiota in mice. These changes are attributed in part to reduced food consumption. Fecal transfer experiments demonstrate that the IAV-conditioned microbiota compromises lung defenses against pneumococcal infection. In mechanistic terms, reduced production of the predominant short-chain fatty acid (SCFA) acetate affects the bactericidal activity of alveolar macrophages. Following treatment with acetate, mice colonized with the IAV-conditioned microbiota display reduced bacterial loads. In the context of influenza infection, acetate supplementation reduces, in a free fatty acid receptor 2 (FFAR2)-dependent manner, local and systemic bacterial loads. This translates into reduced lung pathology and improved survival rates of double-infected mice. Lastly, pharmacological activation of the SCFA receptor FFAR2 during influenza reduces bacterial superinfection.
Mots clés
acetate, bacterial superinfection, food restriction, free fatty acid receptor 2, gut microbiota, influenza A virus, macrophages, microbial dysbiosis, short-chain fatty acid
Référence
Cell Rep. 2020 Mar 3;30(9):2934-2947.e6
