Development of artificial liver support system combining with liver cells and Kuppfer cells.

IL-17 A调节嗜中性粒细胞依赖性器官损伤。本研究的目的是确定IL-17 A在缺血再灌注（I/R）后中性粒细胞募集中的作用。评估野生型（WT）和IL-17 A敲除（KO）小鼠。在另一项实验中，在I/R之前给予重组（rm）IL-17 A或rmIL-17 A/F。将分离的库普弗细胞与rmIL-17 A孵育，并测量TNF-α的产生。在这两种模型中，肝损伤的程度在急性期（6 h）表现出相似的水平。相反，在亚急性期（20小时），肝损伤显着减少KO与WT相比。这种肝损伤的减少与趋化因子、粘附分子表达的抑制和中性粒细胞向肝脏浸润的减少有关。用rmIL-17 A显著增加分离的库普弗细胞的TNF-α产生。IL-17 A是启动嗜中性粒细胞诱导的炎症反应和肝损伤的关键调节因子。

IL-17A regulates neutrophil-dependent organ injury. The purpose of this study was to determine the role of IL-17A in neutrophil recruitment after ischemia-reperfusion (I/R). Wild-type (WT) and IL-17A knockout (KO) mice were evaluated. In another experiments, recombinant (rm) IL-17A or rmIL-17A/F were administered before I/R. Isolated Kupffer cells were incubated with rmIL-17A and production of TNF-alpha was measured. The extent of liver injury demonstrated similar levels in the acute phase (6 h) in these two models. In contrast, in the subacute phase (20 h), liver injury were significantly reduced in the KO compared with the WT. This reduction in liver injury was associated with suppression of chemokine, adhesion molecule expression and reduction in infiltration of neutrophils into the liver. TNF-alpha production by isolated Kupffer cells increased significantly with rmIL-17A. IL-17A is a key regulator in initiating neutrophil-induced inflammatory responses and hepatic injury.