Impaired interferon type I signalling in the liver modulates the hepatic acute phase response in hepatitis C virus transgenic mice

J Hepatol. 2009 Aug;51(2):271-8. doi: 10.1016/j.jhep.2009.03.014. Epub 2009 Apr 23.

Abstract

Background/aims: The immunomodulatory active hepatitis C virus (HCV) has been shown to interfere with antiviral interferon (IFN) type I functions. The aim of the study was to determine whether further basic innate immunologic functions are influenced by HCV.

Methods: The acute phase response (APR) was induced in HCV transgenic (tg) mice and C57BL/6J control mice using lipopolysaccharide. Activation of transcription factors, mRNA expression and production of cytokines and acute phase proteins (APP) were determined. IFN type I and tumor necrosis factor (TNF) alpha signalling were investigated after polyI:C or TNF-alpha treatment.

Results: HCV tg mice showed an attenuated APR: hepatic activation of nuclear factor kappa B (NFkappaB) and interferon-stimulated gene factor 3 (ISGF3), hepatic expression of interleukin (IL) 6, IL-10, and IFN-gamma mRNA, serum concentrations of IL-6 and IFN-gamma and production of type II acute phase proteins were reduced compared to wild-type mice. While no differences in NFkappaB activation could be detected after TNF-alpha injection, HCV tg mice showed reduced activation of ISGF3 and reduced transactivation of IFN target genes after polyI:C treatment.

Conclusions: Besides antiviral defence mechanisms, interruption of IFN type I signalling by HCV modulates the APR which is aimed at a variety of pathogens.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute-Phase Proteins / metabolism
  • Acute-Phase Reaction / genetics
  • Acute-Phase Reaction / immunology
  • Acute-Phase Reaction / physiopathology*
  • Animals
  • Base Sequence
  • Cytokines / blood
  • Cytokines / genetics
  • DNA Primers / genetics
  • Female
  • Hepacivirus / genetics
  • Hepacivirus / immunology*
  • Hepacivirus / pathogenicity*
  • Hepatitis C Antigens / genetics
  • Interferon Type I / physiology*
  • Interferon-Stimulated Gene Factor 3 / metabolism
  • Lipopolysaccharides / toxicity
  • Liver / physiopathology*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • NF-kappa B / metabolism
  • Signal Transduction
  • Tumor Necrosis Factor-alpha / physiology
  • Viral Core Proteins / genetics
  • Viral Core Proteins / immunology

Substances

  • Acute-Phase Proteins
  • Cytokines
  • DNA Primers
  • Hepatitis C Antigens
  • Interferon Type I
  • Interferon-Stimulated Gene Factor 3
  • Lipopolysaccharides
  • NF-kappa B
  • Tumor Necrosis Factor-alpha
  • Viral Core Proteins