16S rRNA Raw sequence reads

Desulfovibrio (DSV), as sulfate-reducing bacteria in the gut microbiota, exerts a pleiotropic effects in host health. Although intestinal overgrowth of DSV expands the bile acid (BA) pool and promotes liver injury, its causal role in hepatic patho-physiology remains incompletely defined. Here we show that DSV-driven liver in-jury is mediated by aberrant BA metabolism coupled with gut microbial remodelling. Cholic acid (CA) alone induced overt hepatic damage, whereas supplemental DSV did not further exacerbate injury caused by excessive CA. Intervention with the BA sequestrant cholestyramine markedly reversed DSV-elicited liver injury, confirming BA-dependent toxicity. Hepatic expression of BA-synthetic genes Cyp7a1 and Cyp8b1 verified a negative-feedback loop of BA metabolism. 16S rRNA gene se-quencing revealed that elevated BA and DSV led to significant changes in the com-position of the intestinal microbiota in mice. Principal Coordinates Analysis (PCoA) revealed a clear separation between the control group and the CA and DSV-CA groups, indicating BA-driven remodelling. Furthermore,we identified several key biomarkers associated with DSV-modulated BA metabolism, including increased abundances of Eubacterium_fissicatena and Enterorhabdus, as well as decreased levels of Intestiniimonas.Collectively, our data demonstrate that abnormal elevation of intestinal BA levels constitutes a key mechanism by which Desulfovibrio triggers liver injury.