Fig. 6

Inhibition of AHR abrogated the protective effects of 5-HIAA supplementation on EAP mice fed an HSD. a AHR levels in prostate tissues of mice among the Ctrl + NSD, Ctrl + HSD, EAP + NSD, EAP + HSD, and EAP + HSD + 5-HIAA groups (n = 4). b A simple schematic diagram of the experimental workflow. c HE staining and inflammation scores of prostate tissues (scale bar = 100 μm, n = 4). d Tactile allodynia development in the mice from the Ctrl + NSD, Ctrl + HSD, EAP + NSD, EAP + HSD, EAP + HSD + 5-HIAA, and EAP + HSD + 5-HIAA + CH groups (n = 4). e The levels of IL-1β, TNF-α, and IL-17A in the serum of the mice in the 6 groups (n = 4). f Proportion of Th17 of CD4⁺ T cells, as determined by flow cytometry, among the splenic lymphocytes of immunized mice in the 6 groups (white arrowheads, n = 4). g The infiltration of Th17 cells in prostate tissues from mice was evaluated by immunofluorescence (scale bar = 100 μm, n = 4). ^*P < 0.05, ^**P < 0.01, ^***P < 0.001, ^****P < 0.0001; ns non-significant. NOD nonobese male diabetic/LtJ, BF breeding feed, EAP experimental autoimmune prostatitis, HSD high-salt diet, NSD normal-salt diet, CH CH223191 (an AHR inhibitor), HE hematoxylin–eosin, IL-1β interleukin-1β, TNF-α tumor necrosis factor-α, IL-17A interleukin-17A, 5-HIAA 5-hydroxyindole acetic acid, AHR aryl hydrocarbon receptor, DAPI 4',6-diamidino-2-phenylindole