摘要：We have been investigating an apoptosis induction in human fetal membrane cells by influenza virus (IV) infection and the contribution of apoptosis induction to the viral infection-defense response between a fetus and the maternal body. For studying any role of uterine cells in the anti-viral response, we investigated the molecular mechanism of the apoptotic induction in human uterine cervical fibroblast cell line (HCF) by IV infection. IV type A and B infection induced DNA fragmentation in HCF. In IV-infected HCF, gene mRNA expression levels of interleukine (IL)-1β, IL-6, tumor necrosis factor (TNF) α, Fas ligand, interferon regulatory factor (IRF)-1, interferon (IFN) α and IFN β increased as compared with those in mock treatment cells, and the induction of mRNAs for double stranded RNA dependent protein kinase (PKR), indolamine 2,3-deoxygenase (IDO) and 2′-5′ oligoadenylate synthetase (2-5 OAS) were indicated, which had a role for a host defense response induced by IFN-β. The amount of IFN-β protein increased by IV-infection, and DNA fragmentation was inhibited with anti-IFN-β antibody and PKR inhibitor (2-aminopurine). Furthermore, a synthetic double stranded RNA, poly I : C, could induce almost the same phenomena as that induced by virus infection. We conclude that IV-infection induces the apoptosis in HCF cells through the IFN-β expression regulated by double stranded RNA and IRF-1 induction, and suggest that the IFN-β induction may be the predominant contribution to the IV infection induced HCF apoptosis.
