沙眼衣原体抑制宿主细胞凋亡机制的研究进展  

Advances in inhibition apoptosis mechanism for host cell from chlamydia trachomatis

作　　者：雷文波[1] 何战胜[1] 李忠玉[1] 

机构地区：[1]南华大学病原生物学研究所,湖南衡阳421001

出　　处：《微生物学免疫学进展》2016年第1期62-65,共4页Progress In Microbiology and Immunology

基　　金：国家自然科学基金(81102230;31470277);湖南省高校创新平台开放基金(13K081);湖南省高层次卫生人才"225"工程培养项目(2013-34);湖南省普通高等学校学科带头人项目基金(2014-86)

摘　　要：沙眼衣原体是一类具有独特发育周期的革兰阴性病原体,能够引起人类多种疾病。沙眼衣原体感染的宿主细胞能够抵抗多种凋亡刺激,并且通过抑制宿主细胞凋亡从而完成自身的复制与发育。其抗凋亡机制可能与其参与调节宿主细胞MAPK信号途径、抑制线粒体细胞色素c的释放、上调凋亡抑制蛋白IAPs和降解促凋亡蛋白等多种机制有关。最新研究发现沙眼衣原体可以通过HDM2/MDM2与p53相互作用,促进p53蛋白水解,抑制细胞凋亡,从而导致持续性感染。Chlamydia trachomatis is a kind of gram-negative pathogen which has an unique development cycle,it can cause a variety of human diseases. The host cells infected by chlamydia trachomatis can resist to a number of apoptotic stimulation,and chlamydia trachomatis completes its replication and development by inhibiting apoptosis of host cells. Chlamydia trachomatis may be associated with such an anti-apoptotic mechanism involved in the regulation of host cell MAPK signaling pathways,inhibition of mitochondrial cytochrome c release,upregulation of apoptosis inhibitory protein IAPs and degradation proapoptotic proteins. The latest discovery showed that chlamydia trachomatis promotes p53 proteolysis,inhibits apoptosis,and leading to a persistent infection by means of p53 and HDM2 / MDM2 interaction.

关 键 词：沙眼衣原体 细胞凋亡 p53-HDM2/MDM2 丝裂原活化蛋白激酶 凋亡抑制因子 

分 类 号：R374[医药卫生—病原生物学]