Gut microbiota and metabolite interface-mediated hepatic inflammation

Abstract

Immunologic and metabolic signals regulated by gut microbiota and relevant metabolites mediate bidirectional interaction between the gut and liver. Gut microbiota dysbiosis, due to diet, lifestyle, bile acids, and genetic and environmental factors, can advance the progression of chronic liver disease. Commensal gut bacteria have both pro- and anti-inflammatory effects depending on their species and relative abundance in the intestine. Components and metabolites derived from gut microbiota–diet interaction can regulate hepatic innate and adaptive immune cells, as well as liver parenchymal cells, significantly impacting liver inflammation. In this mini review, recent findings of specific bacterial species and metabolites with functions in regulating liver inflammation are first reviewed. In addition, socioeconomic and environmental factors, hormones, and genetics that shape the profile of gut microbiota and microbial metabolites and components with the function of priming or dampening liver inflammation are discussed. Finally, current clinical trials evaluating the factors that manipulate gut microbiota to treat liver inflammation and chronic liver disease are reviewed. Overall, the discussion of microbial and metabolic mediators contributing to liver inflammation will help direct our future studies on liver disease.

The Mediating Effect of 3-Methoxytyrosine on TWEAK Levels and Primary Sclerosing Cholangitis: A Genetic Perspective

“…There is a close correlation between in ammatory-related proteins and metabolites. Numerous studies have shown that gut ora metabolites can promote the expression of in ammation-related proteins and the development of PSC (Yang et al 2024). Conversely, research has also indicated that in ammation-related proteins, such as IFN-γ and TNFα, pro-in ammatory cytokines, can stimulate indoleamine 2,3-dioxygenase to promote the metabolism of tryptophan into kynurenine.…”