Fig. 7From: Gut microbial metabolite deoxycholic acid facilitates Th17 differentiation through modulating cholesterol biosynthesis and participates in high-fat diet-associated colonic inflammationDCA administration enhances Th17 immune response and exacerbates TNBS-induced colitis. a Animal treatment procedure (n = 7 per group). b Representative HE staining and c histological score of colon sections from ND, DCA, ND + TNBS and DCA + TNBS treated mice (n = 4–6). Scale bar, 100 µm (×200) and 50 µm (×400). d The percentage of IL-17-producing cells from mesenteric lymph nodes of ND, DCA, ND + TNBS and DCA + TNBS treated mice. e RORγt (green) and DAPI (blue) immunofluorescence analysis of colon sections from ND, DCA, ND + TNBS and DCA + TNBS treated mice (Scale bar, 50 µm). ***p < 0.001; ****p < 0.0001 compared to the normal diet control mice. ##p < 0.01 compared to the DCA + TNBS treated mice. One-way ANOVA with Newman-Keuls multiple comparisons test (c) was used. Data are expressed as mean ± SEM from at least three independent experiments or representative data (b, d, e)Back to article page