High-Salt Diet Induces IL-17-Dependent Gut Inflammation and Exacerbates Colitis in Mice

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dc.creatorSarah Leao Fiorini de Aguiar
dc.creatorValbert Nascimento Cardoso
dc.creatorPatrícia Aparecida Barros
dc.creatorTatiani Uceli Maioli
dc.creatorAna Maria Caetano Faria
dc.creatorMariana Camila Gonçalves Miranda
dc.creatorMauro Andrade Freitas Guimarães
dc.creatorHelton Costa Santiago
dc.creatorCamila Pereira Queiroz
dc.creatorPricila da Silva Cunha
dc.creatorDenise Carmona Cara
dc.creatorGiselle Foureaux
dc.creatorAnderson José Ferreira
dc.date.accessioned2024-03-20T20:09:40Z
dc.date.accessioned2025-09-08T22:55:40Z
dc.date.available2024-03-20T20:09:40Z
dc.date.issued2018-01-14
dc.description.sponsorshipCNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológico
dc.description.sponsorshipFAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Gerais
dc.description.sponsorshipCAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
dc.format.mimetypepdf
dc.identifier.doihttps://doi.org/10.3389/fimmu.2017.01969
dc.identifier.issn1664-3224
dc.identifier.urihttps://hdl.handle.net/1843/66191
dc.languageeng
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofFrontiers in Immunology
dc.rightsAcesso Aberto
dc.subjectCélulas Th17
dc.subjectInflamação
dc.subjectInterleucina-17
dc.subjectCloreto de Sódio
dc.subject.otherSodium chloride
dc.subject.otherGut inflammation
dc.subject.otherIL-17
dc.subject.otherTh17 cells
dc.subject.otherILC3
dc.titleHigh-Salt Diet Induces IL-17-Dependent Gut Inflammation and Exacerbates Colitis in Mice
dc.typeArtigo de periódico
local.citation.epage12
local.citation.spage1969
local.citation.volume8
local.description.resumoExcess intake of sodium is often associated with high risk for cardiovascular disease. More recently, some studies on the effects of high-salt diets (HSDs) have also demonstrated that they are able to activate Th17 cells and increase severity of autoimmune diseases. The purpose of the present study was to evaluate the effects of a diet supplemented with NaCl in the colonic mucosa at steady state and during inflammation. We showed that consumption of HSD by mice triggered a gut inflammatory reaction associated with IL-23 production, recruitment of neutrophils, and increased frequency of the IL-17-producing type 3 innate lymphoid cells (ILC3) in the colon. Moreover, gut inflammation was not observed in IL-17–/– mice but it was present, although at lower grade, in RAG−/− mice suggesting that the inflammatory effects of HSD was dependent on IL-17 but only partially on Th17 cells. Expression of SGK1, a kinase involved in sodium homeostasis, increased 90 min after ingestion of 50% NaCl solution and decreased 3 weeks after HSD consumption. Colitis induced by oral administration of either dextran sodium sulfate or 2,4,6-trinitrobenzenesulfonic acid was exacerbated by HSD consumption and this effect was associated with increased frequencies of RORγt+ CD4+ T cells and neutrophils in the colon. Therefore, our results demonstrated that consumption of HSD per se triggered a histologically detectable inflammation in the colon and also exacerbated chemically induced models of colitis in mice by a mechanism dependent on IL-17 production most likely by both ILC3 and Th17 cells.
local.identifier.orcidhttps://orcid.org/0000-0002-7538-3208
local.publisher.countryBrasil
local.publisher.departmentENF - DEPARTAMENTO DE NUTRIÇÃO
local.publisher.departmentENFERMAGEM - ESCOLA DE ENFERMAGEM
local.publisher.departmentFAR - DEPARTAMENTO DE ANÁLISES CLÍNICAS E TOXICOLÓGICAS
local.publisher.departmentICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIA
local.publisher.departmentICB - DEPARTAMENTO DE MORFOLOGIA
local.publisher.initialsUFMG
local.url.externahttps://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2017.01969/full

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