The present paper aims to investigate the role of interleukin 23(IL-23)in facilitating Th1,Th2 and Th17 differentiation during respiratory syncytial virus(RSV)infection of epithelial cells(BEAS-2B). Lymphocytes were treated by supernatants from BEAS-2B cells with RSV or mock infection.Then they were blocked by specific anti-IL-23R antibody,anti-IL-23p19 antibody and p38 mitogen-activated protein kinase(MAPK)inhibitor(SB203580).The concentrations of cytokines such as interferon γ(IFN-γ),IL-4 and IL-17 were detected by enzyme-linked immunosorbent assay(ELISA).The mRNA expressions of transcription factors(t-bet,gata3,rorγ t),signal transducers(stat4,stat6,stat3)were determined by real-time polymerase chain reaction(PCR).The results showed that the concentrations of cytokines(IFN-γ,IL-4 and IL-17)were significantly increased after RSV infection,accompanied with the enhanced expressions of transcription factors.However,these cytokines and transcription factors were significantly decreased when IL-23 pathway was blocked by antibodies.The blockage of p38 MAPK signal pathway showed the same results.The results suggest that IL-23 could facilitate Th1,Th2 and Th17 differentiation in RSV-infected BEAS-2B cells,which might be associated with p38 MAPK signal pathway.%本研究旨在探讨白细胞介素23(interleukin 23,IL-23)在呼吸道合胞病毒(respiratory syncytial virus, RSV)感染支气管上皮细胞 BEAS-2B后对 Th1、Th2和 Th17细胞分化的影响及作用机制.将 RSV感染BEAS-2B后的上清液与淋巴细胞共孵育,并分别阻断IL-23受体(IL-23 receptor,IL-23R)、IL-23p19亚基及p38丝裂原活化蛋白激酶(p38 mitogen-activated protein kinase,p38 MAPK)信号通路.应用酶联免疫吸附试验(enzyme-linked immunosorbent assay,ELISA)检测上清液中细胞因子γ干扰素(interferon γ,IFN-γ)、IL-4、IL-17的浓度.同时,应用实时聚合酶链反应(polymerase chain reaction,PCR)检测相关转录因子(t-bet、gata3、rorγt)和信号转导子(stat4、stat6、stat3)的表达.结果显示,RSV感染后IFN-γ、IL-4和IL-17蛋白表达上调,转录因子及信号转导子的表达也有所增加.阻断IL-23和p38 MAPK信号通路后,Th1、Th2和Th7细胞分泌的细胞因子及转录因子表达均明显下降.结果提示,阻断IL-23后可在基因转导层面抑制RSV感染上皮细胞后诱导的Th1、Th2和Th17细胞分化,此过程可能与p38 MAPK信号通路有关.
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