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

ABSTRACT: Excess 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 ROR?t+ 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.

SUBMITTER: Aguiar SLF

PROVIDER: S-EPMC5775230 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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

Aguiar Sarah Leão Fiorini SLF Miranda Mariana Camila Gonçalves MCG Guimarães Mauro Andrade Freitas MAF Santiago Helton Costa HC Queiroz Camila Pereira CP Cunha Pricila da Silva PDS Cara Denise Carmona DC Foureaux Giselle G Ferreira Anderson José AJ Cardoso Valbert Nascimento VN Barros Patrícia Aparecida PA Maioli Tatiani Uceli TU Faria Ana Maria Caetano AMC

Frontiers in immunology 20180115

Excess 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 react ...[more]

PMID: 29379505

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Project description:People consume more salt than the recommended levels due to poor dietary practices. The effects of long-term consumption of high-salt diets (HSD) on liver fibrosis are unclear. This study aimed to explore the impact of HSD on liver fibrosis. In this study, a carbon tetrachloride (CCL4)-induced liver fibrosis mouse model was used to evaluate fibrotic changes in the livers of mice fed a normal diet (ND) and an HSD. The HSD exacerbated liver injury and fibrosis. Moreover, the protein expression levels of transforming growth factor β (TGF-β), tumor necrosis factor alpha (TNF-α), and monocyte chemoattractant protein 1 (MCP-1) were significantly higher in the HSD group than in the normal group. The proportion of macrophages and activation significantly increased in the livers of HSD-fed mice. Meanwhile, the number of macrophages significantly increased in the small intestinal lamina propria of HSD-fed mice. The levels of profibrotic factors also increased in the small intestine of HSD-fed mice. Additionally, HSD increased the profibrotic chemokines and monocyte chemoattractant levels in the portal vein blood. Further characterization suggested that the HSD decreased the expression of tight junction proteins (ZO-1 and CLDN1), enhancing the translocation of bacteria. Enterococcus promoted liver injury and inflammation. In vitro experiments demonstrated that Enterococcus induced macrophage activation through the NF-κB pathway, thus promoting the expression of fibrosis-related genes, leading to liver fibrogenesis. Similarly, Enterococcus disrupted the gut microbiome in vivo and significantly increased the fibrotic markers, TGF-β, and alpha smooth muscle actin (α-SMA) expression in the liver. IMPORTANCE This study further confirms that Enterococcus induce liver fibrosis in mice. These results indicate that an HSD can exacerbate liver fibrosis by altering the gut microbiota composition, thus impairing intestinal barrier function. Therefore, this may serve as a new target for liver fibrosis therapy and gut microbiota management.

Dataset Information

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

Publications

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

Similar Datasets

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