Cytokines in Steatohepatitis

L. Hammerich, F. Tacke

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

1 Scopus citations

Abstract

Nonalcoholic fatty liver disease (NAFLD) is the leading cause of liver diseases in Western countries and becoming a major health and economic burden. The progression of NAFLD from steatosis to steatohepatitis is causally linked to a massive inflammatory response in the liver, but also associated with signs of systemic inflammation. Cytokines are critically involved in the regulation of immune responses during the progression of NAFLD, and the interplay between systemic and hepatic inflammatory signals is considered as a critical factor in the pathogenesis. Proinflammatory cytokines such as tumor necrosis factor alpha (TNFα), interleukin (IL) 6, IL8, or IL17 contribute to disease progression, while the anti-inflammatory IL10 is associated with protection. In addition, stimulation of toll-like receptors leads to activation of the inflammasome and release of IL1β, contributing to fibrogenesis and inflammation in the liver. This chapter summarizes the major findings regarding the functional role of cytokines in the development of steatohepatitis.

Original languageEnglish
Title of host publicationLiver Pathophysiology
Subtitle of host publicationTherapies and Antioxidants
PublisherElsevier
Pages159-168
Number of pages10
ISBN (Electronic)9780128043219
ISBN (Print)9780128042748
DOIs
StatePublished - 23 Mar 2017
Externally publishedYes

Keywords

  • Cytokines
  • Fatty liver
  • Fibrosis
  • Interferon
  • Interleukin
  • Steatohepatitis
  • Steatosis
  • TNF

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