2型登革病毒诱导ED25细胞凋亡及死亡受体的表达变化

Dengue virus type 2 induces apoptosis and expression of death receptor in hepatic veno-endotheliocyte ED25

目的:观察2型登革病毒(dengue virus type 2,DV2)感染ED25(人肝静脉内皮细胞)诱导细胞凋亡及胞膜死亡受体TRAILR、TNFR、Fas表达水平的改变,并探讨其意义。方法:用DV2感染ED25细胞,流式细胞技术检测ED25细胞感染前、后凋亡变化及胞膜死亡受体TRAILR1-4、TNFR1-2、Fas的表达。结果:病毒感染后ED25细胞凋亡增加,感染前细胞凋亡数约5.7%±1.2%,而感染后细胞凋亡数约27.3%±1.6%,P<0.05;病毒感染后细胞Fas表达百分比增加,感染前为44.3%±2.2%,而感染后为63.0%±2.3%,P<0.05;而TRAILR1-4、TNFR1-2表达水平甚低,感染前后无明显改变。结论:2型登革病毒感染可以诱导肝静脉内皮细胞ED25细胞凋亡,其中死亡受体Fas表达增高,提示DV2可能通过调节Fas/FasL的表达诱导细胞凋亡,有利于进一步研究登革病毒感染引起肝脏器官损伤。

AIM： To investigate apoptosis and the expression of death receptors of TRAIL, TNF and Fas on hepatic veno -endotheliocyte ED25 cell strain induced by dengue virus type 2（DV2）. METHODS： Flow cytometric analysis was used to detect the number of apoptotic cells and the expression levels of TRAILR1 - 4 , TNFR1 - 2, Fas on ED25 cells before/after DV2 infection. RESULTS： The numbers of apoptotic ceils of ED25 increased after DV2 infection, there were only about 5.7% ± 1.2% of apoptotic cells before virus infection while there were approximately 27.3% ± 1.6% of apoptotic cells after virus infection. At the same time the expression level of Fas also increased, before virus infection about 44.3% ± 2. 2% of ED25 ceils expressed Fas while 63.0% ± 2.3% of ED25 cells expressed Fas after virus infection. CONCLUSION： DV2 infection can induce apoptosis of ED25 cells, and it suggests strongly that Fas/FasL may be involved in the apoptotic signal transduction.