regulates gut microbiota and ameliorates the alcoholic-associated liver disease in mice.

INTRODUCTION

Alcoholic-associated liver diseases (ALD) are now widespread issues worldwide. Alcoholic-induced chronic dysbiosis of the gut microbiota is one of the factors in the pathophysiology of ALD.

METHODS

In this work, we employed a chronic-binge ethanol feeding mice model, as described in a previous report.

RESULTS

Our findings demonstrate that hepatic inflammatory injury damage and accumulation of fat can be effectively reduced in mice with ALD by altering the gut microbiota utilizing . Treatment with significantly modulates the levels of TNF-α, IL-1β, and IL-22 cytokines while maintaining tight junction proteins and mucin protein expressions to support intestinal barrier function restoration. Treatment with also alters the composition of the gut microbiota and increases the production of short-chain fatty acids (SCFAs).

DISCUSSION

This is mostly due to promotes the growth of bacteria that produce SCFAs, such as species and , while inhibiting the growth of pathogenic bacteria like . Moreover, treatment with causes levels of , , and increase while and metabolites decrease significantly. This study facilitates the development of therapeutic and preventive strategies for ALD using lactic acid bacteria.