FXR‐Mediated Atherosclerosis Alleviation by <i>B. animalis</i> F1‐7 Through Bile Acid Metabolism‐Driven Gut–Liver Axis Modulation

ABSTRACT This study investigates the mechanisms of B. animalis F1‐7 improving atherosclerosis (AS) through bile acid metabolism by using an “antibiotic cocktail” approach in AS model mice. It was found that B. animalis F1‐7 could effectively reduce lipid accumulation in the aorta of mice, alleviate inflammatory responses and improve the intestinal barrier. Antibiotic intervention partially counteracted the improvement effect of the strain. B. animalis F1‐7 significantly increased the abundance of Bacteroidetes compared with the model group, and the antibiotic intervention affected the beneficial effects of the strain. B. animalis F1‐7 significantly increased the Lactobacillus and Faecalibaculum , and decreased the Coriobacteriaceae UCG‐002 . Analysis of microbial–bile acid correlations showed positive correlations between Coriobacteriaceae_UCG‐002 and deoxycholic acid, lithocholic acid, taurocholic acid, and allantoinic acid, while showing negative correlations with ursodeoxycholic acid and 23‐N‐deoxycholic acid. Both Lactobacillus and Faecalibaculum exhibit negative correlations with deoxycholic acid, lithocholic acid, taurocholic acid, and glycocholic acid. Notably, Lactobacillus also shows positive correlation with ursodeoxycholic acid and 23‐N‐deoxycholic acid. Further analysis at the genetic level confirmed that after the intervention of the strain, the expression of FXR in the intestine was significantly decreased. In contrast, the expression of CYP7A1 in the liver was increased through the regulation of the gut‐liver axis The antibiotic intervention counteracted this effect, demonstrating that the microbiota plays a crucial role in the regulation. Research demonstrates that B. animalis F1‐7 can regulate gut microbiota structure to influence bile acid composition, thereby engaging in the FXR/FGF15/CYP7A1 pathway.