呼吸道合胞病毒抑制JAK/STAT信号通路减少干扰素-β的表达

Inhibition of Interferon-Beta Expression Through Regulating JAK/STAT Signal Pathway in Hep2 Cells Infected with Respiratory Syncytial Virus

目的:探讨呼吸道合胞病毒(RSV)感染上皮细胞早期对酪氨酸蛋白激酶/信号传导与转录活化因子(JAK/STAT)信号通路和β干扰素(IFN-β)表达的影响。方法:RSV体外感染人喉癌上皮细胞(Hep2)0,1,2,4,8,12,24 h后分别应用酶联免疫吸附法(ELISA)和逆转录-聚合酶链反应(RT-PCR)检测感染后各个时间段IFN-β的浓度以及STAT1、STAT2 mRNA的表达水平。结果:RSV感染Hep2细胞后,IFN-β浓度于第2小时后略有上升,但与未感染细胞基础水平无差异性变化(P>0.05)。STAT1、STAT2 mRNA表达第1小时即上升,第2小时达峰值,随后逐渐下降,在第24小时达最低值(P<0.05)。结论:RSV感染Hep2细胞早期上调STAT1、STAT2 mR-NA,继而抑制其转录,对上皮细胞IFN-β的分泌无明显影响。

Objective： To explore the role of JAK/STAT signal pathway in regulating host innate immune response to respiratory syncytial virus （RSV） infection. Methods： Hep2 cells were infected with RSV in vitro, and the supernatants and cells were harvested at 0,1,2,4,8,12,24 h post-infection respectively. Then enzyme-linked immunosorbent assay （ELISA） and reverse transcription PCR （RT-PCR） were performed to detect the expression of IFN-β and the transcription of STAT1/2 mRNA. Results： The expression of STAT1/2 mRNA increased at 2 h post-infection （P〈0.05） and decreased dramatically in 2-24 hours post-infection. However, within 24 h postinfection by RSV, there was no significant change of IFN-βexpression （P〉0.05）. Conclusion： RSV plays a different role in the regulation of STAT1/2 expression by up-regulating in the early stage of infections, and down-regulating in 2 24 hours post-infection, while does not activate the expression of IFN-β.