猪链球菌2型溶菌酶释放蛋白诱导血管内皮细胞融合  

Fusion of Microvascular Endothelial Cells Induced by Muramidase-Released Protein of Streptococcus suis Type 2

作　　者：曾巧英[1,2] 陆承平[1] 

机构地区：[1]南京农业大学农业部动物疫病诊断与免疫重点开放实验室 [2]甘肃农业大学动物医学院,兰州730070

出　　处：《中国农业科学》2005年第4期821-825,共5页Scientia Agricultura Sinica

基　　金：国家"973"资助项目(G1999011906)

摘　　要：猪链球菌2型(SS2)主要引起人和猪的脑膜炎,但其毒力因子溶菌酶释放蛋白(MRP)对构成血脑屏障的微血管内皮细胞有何致病作用迄今不明。为此分离仔兔脾微血管内皮细胞(SMEC),纯化后用SV40-T 抗原转化后用作试验的细胞模型。将单层SMEC 和电泳纯MRP 溶液共孵育,染色后,光镜观察,发现MRP 可诱导SMEC发生两种典型形态学变化:致密细胞单层中出现巨大空洞而呈网状;空洞内有细胞融合,形成多核巨细胞,随后巨细胞核极度浓缩释出,巨细胞消失。研究结果表明, MRP 单独足以破坏大脑的血管内皮细胞屏障。Streptococcus suis type 2 (SS2) mainly causes meningitis of human and pigs. Muramidase-released protein (MRP) is one of the key virulence factors of SS2. However,the pathogenic effects of MRP on microvascular endothelial cells (MEC) which makes up of brain blood barrier (BBB) is unknown to date. So the spleen microvascular endothelial cells (SMEC) from neonatal rabbit were isolated, purified, immortalized by SV40-T antigen, and used as cell model in present study. After co-incubation with electrophoretically purified MRP, two principal morphologic changes of SMEC confluent layer were revealed by light microscopy. Firstly, the confluent cell layer turned into a riddle-like structure full of giant hole. Secondly, cells were fused into syncytia which scattered in the hole, containing 10～30 nuclei. The nuclei were then released from the syncytia after an extreme condensation. And finally, the syncytia disappeared. Results of present study suggest that MRP alone is sufficient to destroy the brain blood barrier.

关 键 词：猪链球菌2型 溶菌酶释放蛋白 血管内皮细胞 细胞融合 细胞凋亡 脑膜炎 

分 类 号：S852.3[农业科学—基础兽医学]