Fig. 5

C. hiranonis is a diet-responsive species with the ability to ameliorate intestinal disease. a Relative abundance of the OTU corresponding to C. hiranonis (HQ776819.1.1426) in 16S rRNA sequencing data for DR and NDR animals. b Coverage of the bile acid operon (bai) from the C. hiranonis reference (ASM15605v1) with whole genome sequencing reads produced C. hiranonis (teal) and C. perfringens (red) canine clinical isolates. c Bile salt hydrolase (BSH) gene-containing species in DR animals. Pie chart shows the proportion of (BSH) gene-containing species from each genus. d Schematic showing experimental design for mouse experiments. e Weight changes across the experiment (n = 5). f Length of colon at day 8. g Representative H&E staining sections of distal colon tissues at day 8 (× 20 objective) (n = 5 mice). h Inflammation scores estimated from distal colon tissue with H&E staining (n = 5). i Goblet cell numbers in crypts of distal colon, identified with PAS staining. Ten crypts in each section were randomly selected and evaluated only if aligned along the longitudinal axis such that the lumen of the crypt could be seen along its length. j DCA concentration in mouse stools before (day -1) and after (day 3) DSS treatment (n = 4 or 5 mice). k Colony-forming units (CFUs) of E. coli in colon content of mice (n = 5). E. coli was colonized into mice 3 days before DSS treatment (day -3), and the colon lumen content was harvested at day 8. Experiments (d–k) were repeated at least 2 times with similar results. Data shown are from a representative experiment (mean ± sd shown). ns, not significant. *P < 0.05, **P < 0.01, ****P < 0.0001 using the two-sided Wilcoxon signed rank sum test for a and k, and the two-sided t test for e, f, h, i, and j (paired test for j)