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Gut Dysbiosis during Influenza Contributes to Pulmonary Pneumococcal Superinfection through Altered Short-Chain Fatty Acid Production

Sencio, Valentin ; Barthelemy, Adeline ; Tavares, Luciana P. ; Machado, Marina G. ; Soulard, Daphnée ; Cuinat, Céline ; Queiroz-Junior, Celso Martins ; Noordine, Marie-Louise ; Salomé-Desnoulez, Sophie ; Deryuter, Lucie ; Foligné, Benoit ; Wahl, Céline ; Frisch, Benoit ; Vieira, Angelica T. ; Paget, Christophe ; Milligan, Graeme ; Ulven, Trond ; Wolowczuk, Isabelle ; Faveeuw, Christelle ; Le Goffic, Ronan ; Thomas, Muriel ; Ferreira, Stéphanie ; Teixeira, Mauro M. ; Trottein, François

Cell reports (Cambridge), 2020-03, Vol.30 (9), p.2934-2947.e6 [Periódico revisado por pares]

United States: Elsevier Inc

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Título:
Gut Dysbiosis during Influenza Contributes to Pulmonary Pneumococcal Superinfection through Altered Short-Chain Fatty Acid Production
Autor: Sencio, Valentin ; Barthelemy, Adeline ; Tavares, Luciana P. ; Machado, Marina G. ; Soulard, Daphnée ; Cuinat, Céline ; Queiroz-Junior, Celso Martins ; Noordine, Marie-Louise ; Salomé-Desnoulez, Sophie ; Deryuter, Lucie ; Foligné, Benoit ; Wahl, Céline ; Frisch, Benoit ; Vieira, Angelica T. ; Paget, Christophe ; Milligan, Graeme ; Ulven, Trond ; Wolowczuk, Isabelle ; Faveeuw, Christelle ; Le Goffic, Ronan ; Thomas, Muriel ; Ferreira, Stéphanie ; Teixeira, Mauro M. ; Trottein, François
Assuntos: acetate ; Acetates - pharmacology ; Animals ; bacterial superinfection ; Dysbiosis - complications ; Dysbiosis - microbiology ; Dysbiosis - virology ; Fatty Acids, Volatile - biosynthesis ; Feeding Behavior ; food restriction ; free fatty acid receptor 2 ; Gastrointestinal Microbiome - drug effects ; Gastrointestinal Tract - drug effects ; Gastrointestinal Tract - microbiology ; gut microbiota ; Humans ; Immunology ; influenza A virus ; Influenza, Human - microbiology ; Life Sciences ; Lung - microbiology ; macrophages ; Macrophages, Alveolar - drug effects ; Macrophages, Alveolar - microbiology ; Macrophages, Alveolar - pathology ; Mice, Inbred C57BL ; microbial dysbiosis ; Pneumococcal Infections - complications ; Pneumococcal Infections - microbiology ; Pneumococcal Infections - virology ; Receptors, G-Protein-Coupled - agonists ; Receptors, G-Protein-Coupled - metabolism ; Respiratory Tract Infections - microbiology ; short-chain fatty acid ; Superinfection - complications ; Superinfection - microbiology
É parte de: Cell reports (Cambridge), 2020-03, Vol.30 (9), p.2934-2947.e6
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
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Descrição: 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. [Display omitted] •Influenza alters the production of SCFAs by the gut microbiota•The dysbiotic microbiota transfers susceptibility to respiratory bacterial infection•Supplementation with acetate restores the killing activity of alveolar macrophages•Activation of the SCFA receptor FFAR2 protects against bacterial superinfection Sencio et al. provide insights into the mechanisms that underlie bacterial superinfection post-influenza. The authors demonstrate that influenza infection remotely alters the production of short-chain fatty acids (SCFAs) by the gut microbiota. Supplementation with acetate or pharmacological activation of the SCFA receptor FFAR2 reduces susceptibility to secondary bacterial infection.
Editor: United States: Elsevier Inc
Idioma: Inglês

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Gut Dysbiosis during Influenza Contributes to Pulmonary Pneumococcal Superinfection through Altered Short-Chain Fatty Acid Production

United States: Elsevier Inc

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