Analysis of the acute pancreatitis in the mice deficient for the IRF-2 gene

IRF-2基因缺陷小鼠（IRF-2^<-/->小鼠）在polyI：polyC注射或病毒感染后发生急性胰腺炎。IRF-2^<-/->小鼠脾组织中IL-17和IL-22 mRNA的表达明显增加。然而，在体外测定中，IRF-2^<-/->和IRF-2^<+/+> polyI：polyC处理的脾细胞在IL-17和IL-22 mRNA表达水平上没有差异。在骨髓移植分析中，注射polyI：polyC后，具有IRF-2 ^<+/->骨髓的IRF-2 ^<-/->小鼠的血清淀粉酶水平升高。NF-κ B或STAT 3的凝胶位移分析显示IRF-2^<+/+>和IRF-2^<-/->胰腺核提取物之间的不同带型。IRF-2^<+/+>样品中的复合物在IRF-2抗体存在下未发生超位移。免疫印迹法检测IRF-2^<-/->胰腺蛋白中未检测到p65和STAT 3蛋白。结果提示IRF-2^<-/->小鼠胰腺可能是polyI：polyC诱发急性胰腺炎的主要原因。IRF-2^<+/+>和IRF-2^<-/->胰腺之间的微阵列分析目前正在我们实验室进行。polyI：polyC处理的IRF-1^<-/->IRF-2^<-/->双敲除小鼠的血清淀粉酶水平增加与IRF-2^<-/->小鼠相似，但polyI：polyC处理的TRIF^<-/->IRF-2^<-/->小鼠显示血清淀粉酶轻微增加。这些结果表明，RIG-I和MDA 5，而不是IRF-1可能与IRF-2^<-/->小鼠中polyI：polyC诱导的急性胰腺炎有关。在胰腺和皮肤上检测到IL-22受体，但在免疫细胞上未检测到。IL-22受体-/-IRF-2-/-双敲除小鼠的产生正在我们的实验室中进行，我们试图分析这些小鼠的polyI：polyC治疗。

The mice deficient for the IRF-2 gene (IRF-2^<-/-> mice) developed acute pancreatitis after polyI:polyC injection or virus infection. The expression of IL-17 and IL-22 mRNA significantly increased in spleen of IRF-2^<-/-> mice with polyI:polyC injection. However in vitro assay, there was no difference between IRF-2^<-/-> and IRF-2^<+/+> polyI:polyC treated spleen cells in the expression levels of IL-17 and IL-22 mRNA. In bone marrow transplantation analysis, the serum amylase levels increased in IRF-2^<-/-> mice with IRF-2^<+/-> bone marrow after polyI:polyC injection. The gel shift analyses for NF-kB or STAT3 showed the different band-pattern between IRF-2^<+/+> and IRF-2^<-/-> pancreas nuclear extract. The complex from IRF-2^<+/+> sample was not supershifted in the presence of IRF-2 antibody. The proteins of p65 and STAT3 were not detected in IRF-2^<-/-> pancreas protein by the immunoblotting. These results suggested that pancreas from IRF-2^<-/-> mouse may be responsible for the polyI:polyC induced acute pancreatitis. The microarray analysis between IRF-2^<+/+> and IRF-2^<-/-> pancreas is currently underway in our laboratory. The serum amylase level of polyI:polyC treated IRF-1^<-/->IRF-2^<-/-> double knockout mice increased similar to that of IRF-2^<-/-> mice, but polyI:polyC treated TRIF^<-/->IRF-2^<-/-> mice showed slightly increased the serum amylase. These results suggested that RIG-I and MDA5, but not IRF-1 may be related to polyI:polyC induced acute pancreatitis in IRF-2^<-/-> mice. IL-22 receptor is detected on pancreas and skin, but not immune cells. The generation of IL-22 receptor-/-IRF-2-/- double knockout mice is in progress in our laboratory and we attempt to analyze those mice to polyI:polyC treatment.