Fig. 3

TAS1R3 loss protects against WD-induced intestinal inflammation and reduces inflammatory cell infiltration. a qRT-PCR amplification of cDNA from the ileum of Tas1r3^+/+ and Tas1r3^−/− mice (n = 10 mice/group). Ratios of Tas1r3 to Gapdh cycle threshold values are plotted. b Immunohistochemical staining of TAS1R3 in terminal ileum tissue. In vivo experiments (n = 10 mice/group) were performed in triplicate at least twice. Representative c spleens, d small intestines, and e large intestines from diet-induced Tas1r3^+/+ and Tas1r3^−/− mice (n = 10 mice/group). f Hematoxylin and eosin-stained ileal tissue and g tissue injury scores in ND- and WD-fed Tas1r3^+/+ and Tas1r3^−/− mice (n = 10 mice/group). qRT-PCR evaluation of h Il1b, i Il6, and j Tnfα in ileal tissue following diet-induced intestinal inflammation in Tas1r3^+/+ and Tas1r3^−/− mice (n = 10 mice/group). Gapdh was used as the endogenous control. k–n Immunofluorescence and immunohistochemical evaluation of immune cell infiltration in ileal tissue. k CD45⁺ leukocytes, l CD4⁺ T cells, m CD8⁺ T cells, and n CD11b⁺ dendritic cells (n = 10 mice/group). Data represent means ± standard errors of the mean. **P < 0.01 and ****P < 0.0001 (analysis of variance followed by Bonferroni post-hoc test). ND, normal diet; qRT-PCR, quantitative reverse transcription PCR; TAS1R3, taste receptor type 1 member 3; WD, Western diet