A replacement member cytokine IL-33 has recently joined the family of IL-1 due to its 11th number within the family it's also nominated as IL-1F11. In human and mice, main source of IL-33 is liver fibrotic cells and Hepatic stellate cells (HSC) when are in their activated form. To explore the functional role of IL-33 in viral related liver pathology, murine model of hepatitis was developed by injecting Poly I:C and hepatoprotective function of IL-33 was by administration of pre-treatment of mice with recombinant IL-33 (rIL-33). The poly I:C represents a relevant hepatitis model in human, because poly I:C may be a virus-related dsRNA mimetic which plays role in increasing the IL-33 level in fulminant hepatitis. The poly I:C activates the NK cells in liver that results in induction of inflammation. this proposal was to decode the hepatoprotective role of IL-33 and underlying mechanism in viral dsRNA mimetic and poly I:C mediated acute liver diseases i.e. Hepatitis in murine model. Serum biochemical parameters like dosage of aspartate aminotransferase (AST), alanine aminotransferase (ALT) was administered by diagnostic kit in biochemistry autoanalyzer that displayed in higher amount in those mice that were challenged with Poly I:C and therefore the ir level was observed lower in post-treated rIL-33 group after Poly I:C administration and the quantitative measurement of serum INF-γ and TNF-α was performed using Albcam’s INF-γ and TNF-α mice ELISA kits results of both these pro-inflammatory cytokines were same like ALT/AST. Level of those cytokines was also higher in Poly I:C challenged group and lower in post-treated rIL-33 group.
