High salt diet stimulates gut Th17 response and exacerbates TNBS-induced colitis in mice

• DOI: 10.18632/oncotarget.13783
• Publication Date: 2016-12-05T22:00:17Z
• Authors: Yingfeng Wei; Chong Lu; Jianing Chen; Guangying Cui; Lin Wang; Tianming Yu; Yue Yang; Wei Wu; Yulong Ding; Lanjuan Li; Toshimitsu Uede; Zhi Chen; Hongyan Diao
• Keywords: Male; 0301 basic medicine; Interleukin-17; Research Paper: Immunology; Sodium, Dietary; Th1 Cells; Colitis; Inflammatory Bowel Diseases; T-Lymphocytes, Regulatory; Mucosal-Associated Invariant T Cells; Diet; 3. Good health; Disease Models, Animal; Mice; 03 medical and health sciences; Trinitrobenzenesulfonic Acid; Animals; Th17 Cells; Intestinal Mucosa

This study focuses on characterizing the effect of a high salt diet (HSD) on intestinal immunity and the risk of inflammatory bowel diseases (IBD). We found that mice on a HSD had an increased frequency of IL-17A producing cells in the intestinal lamina propria (LP) compared to mice on a normal diet (ND). Furthermore, most intestinal IL-17A producing cells were CD4+TCRβ+ cells. A HSD increased the LP T helper 17 (Th17) responses in both the small and large intestines but did not increase the Th17 response of other gut-associated lymphoid organ. Although, HSD did not change the percentage of regulatory T (Treg) cells, HSD significantly inhibit secretion of IL-10 and the suppressive function of Treg cells. Moreover, we found that HSD exacerbates trinitrobenzenesulfonic acid (TNBS) induced colitis, and Th17 response was significantly increased in the colonic LP of HSD TNBS-treated mice compared with the ND TNBS-treated mice. This study demonstrates that HSD stimulates the intestinal Th17 response but inhibits the function of Treg cells. Moreover, HSD exacerbates TNBS induced mice colitis, suggesting that HSD disrupts the intestinal immunity and increases the risk of IBD.