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目的:探讨呼吸道合胞病毒(RSV)感染上皮细胞中抗病毒信号激活以及细胞因子负调节系统对细胞因子分泌的影响。方法:应用ELISA法检测RSV感染人喉癌上皮细胞(Hep2)培养上清中0,1,2,4,8,12,24 h干扰素α(IFNα-)的浓度;RT-PCR检测病毒感染后各时段上皮细胞内细胞因子信号传导抑制因子(SOCS)1,3和Toll样受体(TLR)3,4的mRNA表达水平。结果:RSV感染上调Hep2细胞SOCS3 mRNA的表达(P<0.05),SOCS1的表达先增高后减低,但无统计学意义;TLR3,TLR4 mRNA的表达增高表现为时间依赖性(P<0.05);IFNβ-的表达在RSV感染后短暂升高而后迅速降低并低于基础表达量(P<0.05)。结论:RSV感染Hep2细胞后上调TLR3,TLR4和SOCS3 mRNA的表达,抑制IFN-α的分泌,提示病毒复制可能通过上调SOCS3而拮抗TLR途径激活的宿主抗病毒免疫应答。
Objective: To investigate the effects of antiviral signal activation and cytokines negative regulation system on the secretion of cytokines in respiratory syncytial virus (RSV) infected epithelial cells. Methods: The concentrations of interferon α (IFNα-) at 0, 1, 2, 4, 8, 12 and 24 h in RSV-infected human laryngeal carcinoma epithelial cells (Hep2) were detected by ELISA. (SOCS) 1, 3 and Toll-like receptor (TLR) 3,4 in epithelial cells at different time points. Results: RSV infection up-regulated the expression of SOCS3 mRNA in Hep2 cells (P <0.05), and the expression of SOCS1 increased first and then decreased, but there was no statistical significance. The expression of TLR3 and TLR4 mRNA increased in a time-dependent manner (P <0.05) - transiently increased after RSV infection and then decreased rapidly and was lower than the basal level (P <0.05). Conclusion: The expression of TLR3, TLR4 and SOCS3 mRNA in Hep2 cells after RSV infection can inhibit the secretion of IFN-α, suggesting that viral replication may antagonize the TLR pathway-activated host anti-viral immune response by up-regulating SOCS3.