Potential role for IL-23 in hepatic ischemia/reperfusion injury

Inflamm Res. 2006 May;55(5):177-8. doi: 10.1007/s00011-006-0073-1.

Abstract

IL-12 and IL-23 are related cytokines that share a p40 subunit. Our previous studies identified IL-12 as a primary initiator of the cytokine cascade induced after hepatic ischemia/reperfusion. Because those studies were conducted prior to the discovery of IL-23, it is not clear whether IL-12 or IL-23 is the relevant cytokine in this response. The current studies show that the antibodies used in our original study cross-react with IL-23. We also found that both IL-12 p35 and IL-23 p19 mRNA are expressed rapidly in the liver after ischemia/reperfusion. Finally, isolated Kupffer cells produced TNFalpha in response to IL-23, but not IL-12, suggesting that IL-23 may be the relevant initiator of the hepatic inflammatory response to ischemia/reperfusion.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Cells, Cultured
  • Gene Expression Regulation
  • Interleukin-12 / biosynthesis
  • Interleukin-12 / genetics
  • Interleukin-12 / pharmacology
  • Interleukin-23
  • Interleukin-23 Subunit p19
  • Interleukins / biosynthesis*
  • Interleukins / genetics
  • Interleukins / pharmacology
  • Kupffer Cells / drug effects
  • Kupffer Cells / metabolism
  • Liver / metabolism*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • RNA, Messenger / biosynthesis
  • Reperfusion Injury / metabolism*
  • Tumor Necrosis Factor-alpha / biosynthesis

Substances

  • Il23a protein, mouse
  • Interleukin-23
  • Interleukin-23 Subunit p19
  • Interleukins
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Interleukin-12