Fig. 2.

Model diagram of the regulatory of IL-17 between gut and hypertension. SCFAs can inhibit HDAC in T cells, which promotes the acetylation of kinase p70 S6 and phosphorylated rS6, thus promoting the mTOR pathway necessary for the proliferation of Th17 cells. HSD could activate the p38/MAPK pathway, involving TonEBP/NFAT5 SGK1 and subsequently mediate the secretion of IL-17a by naive CD4⁺ cells. Moreover, L.murinus can prevent production of Th17 cells induced by HSD. Th17 cells are also mediated by SFB through ROS and SAA. Then IL-17 can promote the reabsorbtion of salt/water and inhibit NO-derived from eNOS, consequently lead to elevation of blood pressure