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

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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.