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Gut microbiota and metabolite interface-mediated hepatic inflammation.
Yang, Ming; Massad, Katina; Kimchi, Eric T; Staveley-O'Carroll, Kevin F; Li, Guangfu.
Afiliação
  • Yang M; Department of Surgery, University of Missouri, Columbia, MO, USA.
  • Massad K; NextGen Precision Health Institute, University of Missouri, Columbia, MO, USA.
  • Kimchi ET; Harry S. Truman Memorial VA Hospital, Columbia, MO, USA.
  • Staveley-O'Carroll KF; Ellis Fischel Cancer Center, University of Missouri, Columbia, MO, USA.
  • Li G; Department of Surgery, University of Missouri, Columbia, MO, USA.
Immunometabolism (Cobham) ; 6(1): e00037, 2024 Jan.
Article em En | MEDLINE | ID: mdl-38283696
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.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article