肺炎支原体表面黏附蛋白的研究进展  

Advances in adhesion proteins of Mycoplasma pneumoniae

作　　者：展磊(综述) 王晓红(审校) ZHAN Lei;WANG Xiaohong(Department of Paediatrics,the First Clinical Medical College,Shanxi Medical University,Taiyuan 030000,Shanxi Province,China)

机构地区：[1]山西医科大学第一临床医学院儿科,山西太原030000

出　　处：《微生物学免疫学进展》2023年第4期76-81,共6页Progress In Microbiology and Immunology

摘　　要：肺炎支原体(Mycoplasma pneumoniae,MP)是社区获得性肺炎的主要病原体之一,MP通过细胞黏附、直接细胞毒性、炎症损伤以及免疫逃逸等途径导致肺炎支原体肺炎(Mycoplasma pneumoniae pneumonia,MPP)。MP的致病性与细胞黏附密切相关,细胞黏附需要一组表面黏附蛋白(surface adhesion protein)共同完成,如P1、P30、P40、P90、P116、P65蛋白,高分子量蛋白(high molecular weight,HMW)1、HMW2、HMW3,延伸因子Tu(elongation factor Tu,EF-Tu)以及J-结构域蛋白(J-domain protein,TopJ)。现就MP主要表面黏附蛋白的研究进展作一概述。Mycoplasma pneumoniae(MP)is one of the major causative agent of community acquired pneumonia,causing Mycoplasma pneumoniae pneumonia(MPP)through mechanisms such as cell adhesion,direct cytotoxicity,inflammatory injury and immune evasion.The pathogenicity of MP is closely related to cell adhesion,which requires a group of adhesion proteins to complete,such as P1,P30,P40,P90,P116,P65,HMW1-3 as well as Elongation factor Tu(EF-Tu),J-domain protein(TopJ).The main adhesion proteins of MP are reviewed in this paper.

关 键 词：肺炎支原体 发病机制 细胞结构 表面黏附蛋白 P1蛋白 免疫反应 

分 类 号：R375.2[医药卫生—病原生物学]