猴免疫缺陷病毒引起多形核嗜中性白细胞凋亡的可能机理(英文)

A Possible Mechanism of Apoptosis Induced by Simian Immunodeficieny Virus in Polymorphonuclear Neutrophils

本实验目的是研究猴免疫缺陷病毒 (SIV)引起多形核嗜中性白细胞 (PMNs)凋亡的机理。实验用PCR技术扩增gag基因 ,用Westernblot法测定p5 3和bcl 2基因的表达。结果显示PMNs在被SIV感染后随着保温时间的延长存活率下降 ,在感染后 2 4h可以从PMNs中扩增出gag基因。PMNs中p5 3基因的的表达在感染后 2 4h增加。同时bcl 2基因的表达在对照组和SIV感染组都增加 ,但在SIV感染组bcl 2蛋白的表达明显低于对照组。结果揭示SIV能够感染PMNs ,p5 3和bcl

The aim of this study is to investigate the mechanisms of apoptosis in polymorphonuclear neutrophils(PMNs) induced by simian immunodeficiency virus(SIV).In this experiment, gag gene was amplified by the polymerase chain reaction and the expression of p53 and bcl 2 gene were determined by Western blot assay.The results showed that the viability of PMNs after treated with SIV was declined as the incubation time prolonged. gag gene could be amplified from PMNs at 24 h postinfection.The expression of p53 gene in PMNs was enhanced at 24 h postinfection.At the same time,the expression of bcl 2 gene were elevated in both of control and SIV infected group,but the production of bcl 2 protein in SIV infected group was obviously lower than control.Our data indicate that PMNs could be infected with SIV and the changed expression of p53 and bcl 2 gene might be one of the mechanisms of apoptosis occurred in PMN infected with SIV.