Role of TLR9 in hepatic stellate cells and experimental liver fibrosis

Biochem Biophys Res Commun. 2008 Nov 14;376(2):271-6. doi: 10.1016/j.bbrc.2008.08.096. Epub 2008 Aug 28.

Abstract

Accumulating evidence indicates that bacteria and bacterial products promote hepatic fibrogenesis. The activation of hepatic stellate cells (HSC) plays a central role in hepatic fibrosis. Here, we demonstrate that HSC express toll-like receptor 9 (TLR9), a pattern recognition receptor that is activated by CpG motifs present specifically in bacterial DNA. Upon CpG stimulation human as well as murine HSC isolated from wild-type (TLR9+/+) mice express increased levels of the profibrogenic chemokine monocyte chemotactic protein 1 (MCP-1). In contrast, HSC isolated from TLR9 deficient (TLR9-/-) mice lacked CpG motif induced MCP-1 expression indicating the functionality of TLR9 in HSC. Bile duct ligation revealed significantly lower hepatic MCP-1 and collagen expression and less hepatic fibrosis in TLR9-/- compared to TLR9+/+ mice. In addition, the expression of hepatic alpha-smooth-muscle actin, a known marker for HSC activation, was reduced in TLR9-/- mice indicating that bacterial DNA induces the activation of HSC and therefore promotes hepatic fibrosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Animals
  • Chemokine CCL2 / genetics
  • CpG Islands / immunology*
  • DNA, Bacterial / immunology*
  • Humans
  • Liver / immunology*
  • Liver / pathology
  • Liver Cirrhosis / immunology*
  • Liver Cirrhosis / pathology
  • Mice
  • Mice, Mutant Strains
  • Models, Animal
  • Toll-Like Receptor 9 / genetics
  • Toll-Like Receptor 9 / immunology*

Substances

  • Actins
  • Chemokine CCL2
  • DNA, Bacterial
  • Toll-Like Receptor 9