Tolerance and sensitization to endotoxin in Kupffer cells caused by acute ethanol involve interleukin-1 receptor-associated kinase

Biochem Biophys Res Commun. 2000 Nov 2;277(3):686-90. doi: 10.1006/bbrc.2000.3738.

Abstract

Ethanol changes sensitivity of Kupffer cells to endotoxin. Here, the hypothesis that interleukin-1 receptor-associated kinase (IRAK), a downstream signaling molecule of toll-like receptors, regulates the response to LPS in Kupffer cells after ethanol treatment was evaluated. C57BL/6 mice were given ethanol intragastrically, and LPS was injected 1 or 21 h later. One hour after ethanol treatment, serum transaminases after LPS were 60% of control, while ethanol increased these parameters about 3-fold 21 h after ethanol. Pretreatment with antibiotics blocked these effects of ethanol. In Kupffer cells from mice treated with ethanol 1 h earlier, LPS-induced TNFalpha production, and IRAK expression and activity and NFkappaB were decreased 50-60% of control. In contrast, in Kupffer cells from mice treated with ethanol 21 h earlier, LPS-induced TNFalpha production, expression and activity of IRAK were increased 1.5-fold over controls, while NFkappaB was elevated 3-fold. These data indicate that ethanol-induced tolerance and sensitization of Kupffer cells to endotoxin in mice involve IRAK.

MeSH terms

  • Animals
  • Ethanol / pharmacology*
  • In Vitro Techniques
  • Interleukin-1 Receptor-Associated Kinases
  • Kupffer Cells / drug effects*
  • Kupffer Cells / enzymology
  • Kupffer Cells / metabolism
  • Lipopolysaccharides / pharmacology*
  • Liver / drug effects*
  • Liver / enzymology
  • Mice
  • Mice, Inbred C57BL
  • Protein Kinases / metabolism*
  • Transaminases / metabolism
  • Tumor Necrosis Factor-alpha / biosynthesis

Substances

  • Lipopolysaccharides
  • Tumor Necrosis Factor-alpha
  • Ethanol
  • Transaminases
  • Protein Kinases
  • Interleukin-1 Receptor-Associated Kinases