Differences in innate immune signaling between alcoholic and non-alcoholic steatohepatitis

J Gastroenterol Hepatol. 2013 Aug;28 Suppl 1(0 1):93-8. doi: 10.1111/jgh.12020.

Abstract

The similar histopathological characteristics of alcoholic steatohepatitis (ASH) and non-alcoholic steatohepatitis (NASH), and the crucial role of the innate immune response in both conditions may lead to the assumption that ASH and NASH represent the same pathophysiological entities caused by different risk factors. In this review paper, we elaborate on the pathophysiological differences between these two entities and highlight the disease-specific involvement of signaling molecules downstream of the Toll-like receptor 4, and the differential mechanism by which the inflammasome contributes to ASH versus NASH. Our findings emphasize that ASH and NASH have disease-specific mechanisms and therefore represent distinct biological entities. Further studies are needed to dissect the emerging differences in pathogenesis of these two conditions.

Keywords: Kupffer cells; Toll-like receptors; alcoholic liver disease; alcoholic steatohepatitis; inflammasome; innate immunity; interleukin-1 beta; interleukin-1 receptor antagonist; non-alcoholic steatohepatitis.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Bacteria
  • Fatty Liver / genetics
  • Fatty Liver / immunology*
  • Fatty Liver, Alcoholic / genetics
  • Fatty Liver, Alcoholic / immunology*
  • Humans
  • Immunity, Innate / genetics
  • Immunity, Innate / immunology*
  • Immunity, Innate / physiology
  • Inflammasomes
  • Interleukin-1
  • Intestines / microbiology
  • Lipopolysaccharides
  • Non-alcoholic Fatty Liver Disease
  • Risk Factors
  • Signal Transduction / genetics
  • Signal Transduction / immunology*
  • Signal Transduction / physiology
  • Toll-Like Receptor 4

Substances

  • Inflammasomes
  • Interleukin-1
  • Lipopolysaccharides
  • Toll-Like Receptor 4