Journal
ONCOTARGET
Volume 8, Issue 1, Pages 70-82Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.13783
Keywords
high salt diet; Th17 cells; regulatory T cells; inflammatory bowel diseases; intestinal immunity; Immunology and Microbiology Section; Immune response; Immunity
Categories
Funding
- National Natural Science Foundation of China [81271810, 81571953]
- National Basic Research Program [2013CB531405]
- Zhejiang medical science and technology project [2015118507]
- Zhejiang Provincial Natural Science Foundation of China [LY16H190002]
Ask authors/readers for more resources
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(+)TCR beta(+) 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available