Disruption of the gut-liver axis in the pathogenesis of acute-on-chronic liver failure

Eur J Gastroenterol Hepatol. 2018 Feb;30(2):130-135. doi: 10.1097/MEG.0000000000001026.

Abstract

Acute-on-chronic liver failure (ACLF) is characterized by organ failure mediated by acute decompensation of cirrhosis. Recent studies have highlighted the importance of the gut-liver axis (GLS) and its association with ACLF pathogenesis. In this review, we discuss the mechanisms related to the alteration of the GLA and their involvement in ACLF pathogenesis and suggest some possible therapeutic options that could modulate the GLA dysfunction. This knowledge may provide information useful for the design of therapeutic strategies for gut dysbiosis and its complications in ACLF.

Publication types

  • Review

MeSH terms

  • Acute-On-Chronic Liver Failure / immunology*
  • Acute-On-Chronic Liver Failure / metabolism
  • Acute-On-Chronic Liver Failure / microbiology*
  • Adaptive Immunity*
  • Animals
  • Bacterial Translocation
  • Dendritic Cells / immunology
  • Dietary Supplements
  • Dysbiosis / drug therapy*
  • Gastrointestinal Microbiome
  • HMGB1 Protein / antagonists & inhibitors
  • Humans
  • Immunity, Innate*
  • Intestinal Mucosa / immunology*
  • Intestinal Mucosa / physiopathology
  • Lipopolysaccharides / immunology
  • Protein Kinase Inhibitors / therapeutic use
  • Toll-Like Receptor 4 / antagonists & inhibitors
  • c-Mer Tyrosine Kinase / antagonists & inhibitors

Substances

  • HMGB1 Protein
  • Lipopolysaccharides
  • Protein Kinase Inhibitors
  • TLR4 protein, human
  • Toll-Like Receptor 4
  • MERTK protein, human
  • c-Mer Tyrosine Kinase