结肠炎
促炎细胞因子
炎症性肠病
钠
TLR4型
炎症
发病机制
食欲
免疫学
化学
免疫系统
细胞因子
内科学
内分泌学
医学
疾病
有机化学
作者
Alan L. Tubbs,Бо Лю,Troy D. Rogers,R. Balfour Sartor,Edward A. Miao
出处
期刊:Journal of Immunology
[The American Association of Immunologists]
日期:2017-06-22
卷期号:199 (3): 1051-1059
被引量:67
标识
DOI:10.4049/jimmunol.1700356
摘要
Abstract The Western diet is characterized by high protein, sugar, fat, and low fiber intake, and is widely believed to contribute to the incidence and pathogenesis of inflammatory bowel disease (IBD). However, high sodium chloride salt content, a defining feature of processed foods, has not been considered as a possible environmental factor that might drive IBD. We set out to bridge this gap. We examined murine models of colitis on either a high salt diet (HSD) or a low salt diet. We demonstrate that an HSD exacerbates inflammatory pathology in the IL-10–deficient murine model of colitis relative to mice fed a low salt diet. This was correlated with enhanced expression of numerous proinflammatory cytokines. Surprisingly, sodium accumulated in the colons of mice on an HSD, suggesting a direct effect of salt within the colon. Similar to the IL-10–deficient model, an HSD also enhanced cytokine expression during infection by Salmonella typhimurium. This occurred in the first 3 d of infection, suggesting that an HSD potentiates an innate immune response. Indeed, in cultured dendritic cells we found that high salt media potentiates cytokine expression downstream of TLR4 activation via p38 MAPK and SGK1. A third common colitis model, administration of dextran sodium sulfate, was hopelessly confounded by the high sodium content of the dextran sodium sulfate. Our results raise the possibility that high dietary salt is an environmental factor that drives increased inflammation in IBD.
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