EV71型手足口病患儿外周血树突状细胞及细胞因子产生的调节机制研究

On regulatory mechanisms of inflammatory cytokines and dendritic cell of HFMD infected with intestinal virus EV71

目的探讨肠道病毒EV71型感染对树突状细胞(DC)成熟凋亡、DC中信号传导通路激活、细胞因子释放的作用机制。方法收集肠道病毒EV71型感染患儿40例,分为20例轻症型组及20例重症型组,正常对照组儿童20例。流式细胞仪检测各组儿童外周血DC表面标志分子CD11c、CD86、CD80和CD83表达的百分比;采用Western blot法检测DC中MAPK信号传导通路分子磷酸化水平;ELISA法检测同期血清中细胞因子的水平。结果随着EV71感染程度的加深,外周血DC中标志着细胞成熟的表面标志分子水平均有增加,CD83及CD80尤为显著;MAPK信号传导通路的活化程度逐渐加强;细胞因子水平的表达显著升高。结论 EV71感染可促进树突状细胞成熟凋亡、激活MAPK信号传导通路并增加细胞因子的释放,MAPK信号传导通路在EV71感染的DC中发挥显著调控作用。

Objective To study maturation, apoptosis, signal pathway and inflammatory cytokines of dendritic cell when infected with intestinal virus EV71. Methods Patients were divided into three groups according to the degree of infection ： the control group （ n = 20）, the mild group （ n = 20） and the severe group （ n = 20）. The percentage of CD11e, CD86, CDS0 and CD83 expression in peripheral blood DC were detected by flow cytometry; the phos- phorylation of MAPK signal transduction pathway in DC was detected by Western blot ; the serum levels of cytokines were measured by ELISA. Results With the increase of the EVTl infection severity, percentage of the marker molecule that marks the surface of cells maturing in peripheral blood DC increased, especially CD83 and CDS0. The activation of MAPK signal transduction pathway gradually increased; the expression of cytokine level were sig- nificantly increased. Conclusion EVT1 infection can promote dendritic cell maturation and cytokine secretion.