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Microbiota-derived acetate protects against respiratory syncytial virus infection through a GPR43-type 1 interferon response

dc.contributor.authorAntunes, Krist Helen
dc.contributor.authorFachi, Jose Luis
dc.contributor.authorde Paula, Rosemeire
dc.contributor.authorda Silva, Emanuelle
dc.contributor.authorPral, Lais Passariello
dc.contributor.authordos Santos, Adara Aurea
dc.contributor.authorDias, Greicy Brisa Malaquias
dc.contributor.authorVargas, Jose Eduardo
dc.contributor.authorPuga, Renato
dc.contributor.authorMayer, Fabiana Quoos
dc.date.accessioned2020-06-19T17:38:26Z
dc.date.available2020-06-19T17:38:26Z
dc.date.issued2019-07-22
dc.identifier.citationAntunes, K.H., Fachi, J.L., de Paula, R. et al. Microbiota-derived acetate protects against respiratory syncytial virus infection through a GPR43-type 1 interferon response. Nat Commun 10, 3273 (2019). https://doi.org/10.1038/s41467-019-11152-6en_US
dc.identifier.issn2041-1723
dc.identifier.urihttp://hdl.handle.net/1803/10057
dc.description.abstractSevere respiratory syncytial virus (RSV) infection is a major cause of morbidity and mortality in infants <2 years-old. Here we describe that high-fiber diet protects mice from RSV infection. This effect was dependent on intestinal microbiota and production of acetate. Oral administration of acetate mediated interferon-beta (IFN-beta) response by increasing expression of interferon-stimulated genes in the lung. These effects were associated with reduction of viral load and pulmonary inflammation in RSV-infected mice. Type 1 IFN signaling via the IFN-1 receptor (IFNAR) was essential for acetate antiviral activity in pulmonary epithelial cell lines and for the acetate protective effect in RSV-infected mice. Activation of Gpr43 in pulmonary epithelial cells reduced virus-induced cytotoxicity and promoted antiviral effects through IFN-beta response. The effect of acetate on RSV infection was abolished in Gpr43(-/-) mice. Our findings reveal antiviral effects of acetate involving IFN-beta in lung epithelial cells and engagement of GPR43 and IFNAR.en_US
dc.description.sponsorshipWe thank Gessica Antunes and Janaina Pasetti for technical assistance. This study was supported by Sao Paulo Research Foundation (FAPESP, 2012/10653-9; 2013/06810-4; 2017/06577-9), FAPERGS (17/2551-0001 380-8), National Council for Scientific and Technological Development (CNPq) (036270/2016), and Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior-Brasil (CAPES)-Finance Code 001.en_US
dc.language.isoen_USen_US
dc.publisherNature Communicationsen_US
dc.rightsThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
dc.source.urihttps://www.nature.com/articles/s41467-019-11152-6#citeas
dc.subjectCHAIN FATTY-ACIDSen_US
dc.subjectGUT MICROBIOTAen_US
dc.subjectDIETARY FIBERen_US
dc.subjectINFLAMMATORY RESPONSESen_US
dc.subjectVIRAL BRONCHIOLITISen_US
dc.subjectINNATE IMMUNITYen_US
dc.subjectGENEen_US
dc.subjectSUSCEPTIBILITYen_US
dc.subjectCELLSen_US
dc.subjectRSVen_US
dc.titleMicrobiota-derived acetate protects against respiratory syncytial virus infection through a GPR43-type 1 interferon responseen_US
dc.typeArticleen_US
dc.identifier.doi10.1038/s41467-019-11152-6


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