Abstract
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.
Highlights
Poor eating habits contribute to various human illnesses and may be considered critical risk factors for diseases such as obesity and cardiovascular disease [1]
IL-17A is considered a signature cytokine of T helper 17 (Th17) cells, IL-17A is secreted by γδ T cells [22], natural killer T (NKT) cells [23], and mucosa-associated invariant T (MAIT) cells, which can be characterized as TCRβ+CD4-CD8-/ lowCD44+ cells in mice [24]
The cell fraction of the innate lymphoid cells (ILCs) in SI lamina propria (LP) IL-17A+ cells was very low and not significantly affected by a high salt diet (HSD) (Figure 1H). These results suggest that a HSD selectively increases IL-17A producing cells in the intestinal LP and that these cells are mainly composed of Th17 cells
Summary
Poor eating habits contribute to various human illnesses and may be considered critical risk factors for diseases such as obesity and cardiovascular disease [1]. It has been well established that excess NaCl intake is closely linked to the development of cardiovascular disease and stroke [5, 6]. There is growing evidence that excess NaCl affects the immune system, leading to an increased incidence of autoimmune diseases [7,8,9]. A recent study revealed that excess consumption of NaCl increases the number of monocyte in the human peripheral blood, and is accompanied by enhanced production of pro-inflammatory cytokines and reduced anti-inflammatory factors [10]. It has been shown that, when compared to a normal salt diet (ND), a HSD increases the severity of www.impactjournals.com/oncotarget experimental autoimmune encephalomyelitis (EAE) in mice accompanied by increased Th17 response [7, 8]
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