Fig 1: B. fragilis induces excessive bile acid synthesis and inhibits hepatic bile acid excretion through suppression of FXR signaling to promote ICP.a Hepatic mRNA expression levels of bile acids synthetic and bile excretory genes in mice transplanted with fecal microbiota of ICP and healthy controls (n = 6 per group). P values were determined by two-tailed Student’s t-test. b Hepatic mRNA expression levels of bile acids synthetic and bile excretory genes in control group, B. fragilis group and EE2 group (n = 6 per group). c Hepatic mRNA expression levels of bile acids synthetic and bile excretory genes in each group (n = 6 per group). P values were determined by Welch ANOVA with Games-Howell’s multiple comparisons test for b, c. d IHC staining of hepatic bile acids synthetic and bile excretory proteins of mice colonized with B. fragilis together with GDCA or not. Scale bar: 20 μm. e Hepatic mRNA expression levels of bile acids synthetic and bile excretory genes in mice colonized with B. fragilis together with GW4064 (10 mg/kg/d) or not (n = 6 per group). f Hepatic mRNA expression levels of bile acids synthetic and bile excretory genes in WT mice or FXR−/− mice colonized with B. fragilis or not (n = 6 per group). P values were determined by Welch ANOVA with Games-Howell’s multiple comparisons test for e, f. g, h Correlations between B. fragilis abundance and FGF19 (g) or C4 (h) were determined by Spearman’s rank test. i Schematic mechanisms underlying the role of the B. fragilis-bile acid-FXR axis in regulating ICP. Data are presented as mean ± SEM for a-c, e, f. Source data are provided as a Source Data file.
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