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This dysregulation sets up a feedback loop where intestinal dysbiosis and altered BA metabolism mutually reinforce each other, driving the progression of ALD.179 For instance, reduced BA secretion during ALD diminishes their bactericidal effect, leading to bacterial overgrowth in the gut.179 Additionally, BA metabolites produced by gut microbiota influence the balance of Th17 cells and Tregs, key immune players in the progression of liver disease.182 Farnesoid X receptor (FXR) is a nuclear receptor that regulates BA synthesis and modulates gut-liver communication.183 When BAs bind to FXR, they inhibit the expression of Cyp7a1/CYP7A1 (cholesterol 7-hydroxylase), a key enzyme in the BA synthesis pathway.180 FXR activation protects the liver from alcohol-induced injury by maintaining gut barrier integrity and limiting gut-derived inflammation.184 However, alcohol impairs FXR function,184 leading to gut barrier dysfunction, dysbiosis and an exacerbation of ALD progression.185 Studies have demonstrated that FXR deficiency, particularly in the intestine rather than in hepatocytes, worsens alcohol-induced liver damage.185 186 This suggests that enhancing FXR activity, especially within the gut, could be a therapeutic strategy for mitigating the harmful effects of alcohol on the liver

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