Lacticaseibacillus paracasei WiKim0110 attenuates alcohol-induced gut–liver axis injury and enhances intestinal barrier-related responses

Abstract

Alcohol consumption disrupts the gut–liver axis by impairing intestinal barrier integrity, altering gut microbiota, and inducing hepatic inflammation. This study investigated whether gut-derived lactic acid bacteria, Lacticaseibacillus paracasei WiKim0110, could attenuate alcohol-induced injury in mice. Alcohol feeding reduced body weight, increased liver weight, and elevated serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, whereas WiKim0110 supplementation significantly ameliorated these alterations. In the large intestine, WiKim0110 supplementation significantly increased the expression of the mucin-related genes Muc2 , Muc3a , and the goblet-cell differentiation factor Atoh1 , while reducing the LPS-sensing markers Tlr4 and Cd14 , suggesting enhancement of mucus barrier-associated responses and attenuation of LPS-associated innate immune signaling. Notably, Lb. paracasei WiKim0110 markedly induced Reg3g expression, suggesting enhanced epithelial antimicrobial defense. Microbiome analysis revealed alcohol-induced dysbiosis characterized by decreased α-diversity and expansion of Escherichia – Shigella , whereas taxa, including Bacteroides , Akkermansia , and Romboutsia , were enriched in the ADW group, suggesting partial restoration of alcohol-induced gut dysbiosis. In the liver, WiKim0110 suppressed inflammatory and lipogenic genes ( Il1b , Fasn , and Acaca ) and enhanced antioxidant-related genes ( Sod1 and Nfe2l2 ). Collectively, these findings suggest that Lb. paracasei WiKim0110 attenuates alcohol-induced gut–liver axis dysfunction and enhances intestinal barrier-related responses.