HSV-1早早期蛋白0对巨噬细胞凋亡及分泌活性的影响

Effect of Expression of HSV-1 Immediately Early Protein 0 on Apoptosis and Secretion of Macrophages

目的研究人单纯疱疹病毒Ⅰ型(HSV-1)早早期蛋白0(ICP0)对巨噬细胞(MΦ)凋亡及分泌活性的影响,为进一步研究ICP0蛋白在HSV-1致病机制中的作用奠定实验基础。方法将真核表达载体PT7-110转染MΦ,以抗ICP0抗体为一抗作Western blot检测其表达。在转染48 h后以ELISA法分析各组培养基中肿瘤坏死因子α(TNF-α)和白细胞介素6(IL-6)产生水平,并收集MΦ经流式细胞术(FCM)检测细胞凋亡。结果 ICP0能够刺激MΦ产生TNF-α和IL-6,且能诱导MΦ发生凋亡。结论 HSV-1 ICP0高表达可诱导MΦ发生凋亡并上调其分泌细胞因子TNF-α和IL-6。

Objective To study the efect of the expression of immediately early protein 0（ICP0）on apoptosis and secretion of macrophages,and to further explore the contribution of ICP0 gene to the infection of HSV-1.Methods Macrophages were transfected with eukaryotic expression vectors PT7-110 and the expression of ICP0 was identified by Western blotting.Macrophages were stimulated with ICP0 to analyze the production of TNF-αand IL-6.The macrophages apoptosis rate was tested by flow cytometry.Result ICP0 stimulated macrophages to produce TNF-α and IL-6 and macrophages apoptosis are also up-regulated in response to ICP0 stimulation.Conclusion The overexpression of ICP0 may induce the apoptosis macrophages and upregulate TNF-α and IL-6 secretion of macrophages.