Lipopolysaccharide signaling induces serum amyloid A (SAA) synthesis in human hepatocytes in vitro

FEBS Lett. 2004 Jul 2;569(1-3):235-9. doi: 10.1016/j.febslet.2004.05.072.

Abstract

To investigate the role of lipopolysaccharide (LPS) in hepatocyte activation, we examined the expression of Toll-like receptor 4 (TLR4), the putative receptor for LPS in human hepatocytes. TLR4 mRNA and protein expression was confirmed in human hepatocytes. Stimulation of human hepatocytes with LPS results in rapid degradation of IkappaB-alpha and mitogen activated protein kinase activation. Human hepatocytes stimulated by LPS produced serum amyloid A protein. Our data suggest that human hepatocytes utilize components of TLR4 signal transduction pathways in response to LPS and these direct LPS-mediated effects on hepatocytes may contribute to liver inflammation and injury.

MeSH terms

  • Cells, Cultured
  • Gene Expression Regulation / drug effects
  • Hepatocytes / drug effects
  • Hepatocytes / metabolism*
  • Hepatocytes / pathology
  • Humans
  • Lipopolysaccharides / pharmacology*
  • Membrane Glycoproteins / genetics*
  • Receptors, Cell Surface / genetics*
  • Serum Amyloid A Protein / biosynthesis*
  • Signal Transduction
  • Toll-Like Receptor 4
  • Toll-Like Receptors
  • Transcription, Genetic / drug effects

Substances

  • Lipopolysaccharides
  • Membrane Glycoproteins
  • Receptors, Cell Surface
  • Serum Amyloid A Protein
  • TLR4 protein, human
  • Toll-Like Receptor 4
  • Toll-Like Receptors