白细胞介素-23在肝脏缺血/再灌注损伤中的潜在作用。

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

作者信息

Husted T L, Blanchard J, Schuster R, Shen H, Lentsch A B

机构信息

The Laboratory of Trauma, Sepsis & Inflammation Research, Department of Surgery, University of Cincinnati College of Medicine, 231 Albert Sabin Way, Cincinnati, Ohio, 45267, USA.

出版信息

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

DOI:10.1007/s00011-006-0073-1

PMID:16830103

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.

摘要

白细胞介素-12（IL-12）和白细胞介素-23（IL-23）是相关的细胞因子，它们共享一个p40亚基。我们之前的研究确定IL-12是肝缺血/再灌注后诱导的细胞因子级联反应的主要启动因子。由于这些研究是在IL-23被发现之前进行的，因此尚不清楚在这种反应中IL-12还是IL-23是相关的细胞因子。目前的研究表明，我们最初研究中使用的抗体与IL-23发生交叉反应。我们还发现，缺血/再灌注后，IL-12 p35和IL-23 p19 mRNA在肝脏中均迅速表达。最后，分离的库普弗细胞对IL-23而非IL-12产生肿瘤坏死因子α（TNFα），这表明IL-23可能是肝脏对缺血/再灌注炎症反应的相关启动因子。