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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 investigate the effects of respiratory syncytial virus (RSV) on epithelial cells in early stage of tyrosine kinase (PKK) / signal transducers and activators of transcription (JAK / STAT) signaling pathway and interferon beta (IFN-β). Methods: Hep2 cells were infected with RSV in vitro for 0, 1, 2, 4, 8, 12 and 24 h after infection with enzyme linked immunosorbent assay (ELISA) and reverse transcription polymerase chain reaction ) To detect the concentration of IFN-β and the expression of STAT1, STAT2 mRNA in each time period after infection. Results: After Hep2 cells were infected with RSV, the concentration of IFN-β increased slightly after 2 hours, but there was no significant difference with the non-infected cells (P> 0.05). STAT1 and STAT2 mRNA expression increased at the first hour, peaked at the second hour, then decreased gradually and reached the lowest level at the 24th hour (P <0.05). CONCLUSIONS: Hep2 cells up-regulated STAT1 and STAT2 mR-NA at the early stage of RSV infection and then inhibited their transcription, which had no significant effect on the secretion of IFN-β by epithelial cells.