Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/351819
Type: Artigo
Title: Acetate coordinates neutrophil and ILC3 responses against C. difficile through FFAR2
Author: Fachi, J.L.
Sécca, C.
Rodrigues, P.B.
de Mato, F.C.P.
Di Luccia, B.
de Souza Felipe, J.
Pral, L.P.
Rungue, M.
de Melo Rocha, V.
Sato, F.T.
Sampaio, U.
Clerici, M.T.P.S.
Rodrigues, H.G.
Câmara, N.O.S.
Consonni, S.R.
Vieira, A.T.
Oliveira, S.C.
Mackay, C.R.
Layden, B.T.
Bortoluci, K.R.
Colonna, M.
Vinolo, M.A.R.
Abstract: Antibiotic-induced dysbiosis is a key predisposing factor for Clostridium difficile infections (CDIs), which cause intestinal disease ranging from mild diarrhea to pseudomembranous colitis. Here, we examined the impact of a microbiota-derived metabolite, short-chain fatty acid acetate, on an acute mouse model of CDI. We found that administration of acetate is remarkably beneficial in ameliorating disease. Mechanistically, we show that acetate enhances innate immune responses by acting on both neutrophils and ILC3s through its cognate receptor free fatty acid receptor 2 (FFAR2). In neutrophils, acetateFFAR2 signaling accelerates their recruitment to the inflammatory sites, facilitates inflammasome activation, and promotes the release of IL-1β; in ILC3s, acetate-FFAR2 augments expression of the IL-1 receptor, which boosts IL-22 secretion in response to IL-1β. We conclude that microbiota-derived acetate promotes host innate responses to C. difficile through coordinate action on neutrophils and ILC3s.
Subject: Neutrófilos
Acetatos
Country: Estados Unidos
Editor: Rockefeller University Press
Rights: Fechado
Identifier DOI: 10.1084/jem.20190489
Date Issue: 2020
Appears in Collections:FEA - Artigos e Outros Documentos

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