Analysis of immunopahtological mechanisms induced by virus infected macrophages.

有许多病毒性疾病是由宿主对感染的免疫应答介导的。其中一些病毒以巨噬细胞为目标。受感染的巨噬细胞迁移并全身传播病毒。此外，巨噬细胞还能分泌大量的炎性细胞因子和趋化因子，并能引起严重的、致命的病理后果。小鼠肝炎病毒（MHV）感染可导致急性、暴发性肝炎和慢性肝炎。急性脑炎和脱髓鞘。本实验研究了MHV感染小鼠腹腔巨噬细胞后，TNF α对巨噬细胞产生炎性细胞因子和趋化因子的影响。TNF α缺陷小鼠IL-1 a和B mRNA表达较野生型C57 BL/6 J小鼠明显降低。为探讨TNF α在MHV致脑炎中的作用，本实验观察了TNF α在TNF α缺陷型B6小鼠（TNFa-/-mice）急性脑炎中的作用。结果提示TNF-α可能不影响JHM诱导的急性致死性脑脊髓炎和两种趋化因子（RANTES和Crg-2）mRNA的表达。

There are many viral disease that are mediated by host immune response to infection. Some of these viruses target at macrophages. Infected macrophages migrate and spread viruses systemically. Moreover, these macrophages secrete massive inflammatory cytokines and chemokines, and are able to cause sever and fatal pathologic consequences.Mouse hepatitis virus (MHV) infection lead to acute and fulmiant hepatitis, chronic hepatitis. acute encephalitis and demyelination in mice. Our previous studies using TNF a deficient mice indicated that TNFa play a important role on the arising of fulminant hepatitis.In this study, we investigated the effect of MHV infection to peritoneal macrophages on production of inflammatory cytokines and chemokines. The mRNA expression of IL-1 a and b of TNF a deficient mice were decreased than that of wild type C57BL/6J mice. It suggested that TNF a affected to the secretion of IL-1.To investigate the role of TNFa on MHV induced encephalitis, we attempted to evaluate its role in acute encephalitis induced MHV-JHM strain infection of TNFa deficient B6 mice(TNFa-/-mice). Our results indicated the possibility that TNF-α did not affect JHM-induced acute lethal encephalomyelitis and two chemokines (RANTES and Crg-2) mRNA expression.