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链球菌的补体抗性机制

Complement resistance mechanisms of streptococci.

作者信息

Jarva Hanna, Jokiranta T Sakari, Würzner Reinhard, Meri Seppo

机构信息

Department of Bacteriology and Immunology, Haartman Institute and HD-Diagnostics, University of Helsinki and Helsinki University Central Hospital, Haartmaninkatu 3, P.O. Box 21, FIN-00290 Helsinki, Finland.

出版信息

Mol Immunol. 2003 Sep;40(2-4):95-107. doi: 10.1016/s0161-5890(03)00108-1.

DOI:10.1016/s0161-5890(03)00108-1
PMID:12914816
Abstract

Group A streptococcus (GAS, Streptococcus pyogenes), group B streptococcus (GBS, Streptococcus agalactiae) and pneumococcus (Streptococcus pneumoniae) are all human pathogens that cause significant morbidity and mortality worldwide. These related species cause different spectra of infections spanning from trivial upper respiratory tract or skin infections to septic and severe diseases. In order to cause deep infections and survive in the human body the bacteria must evade the immune system. Complement is an important part of innate immunity both as an opsonizing and membrane destructing cascade and as an effector system of antibodies. In this review, we describe the complement resistance mechanisms of the three clinically most important streptococcal species, groups A and B streptococci and pneumococcus. The complement evasion mechanisms of these three species are analogous, yet different from one another. Several strains of all three species express molecules (M-proteins, Bac or beta, PspC) that acquire host fluid-phase complement regulators factor H or C4b binding protein to their surfaces. Groups A and B streptococci also secrete proteins and/or enzymes that inhibit the activation of the complement system or chemotaxis caused by the complement activation products. Even though a lot is known about the immune evasion by streptococci, the high morbidity and mortality associated with infections caused by streptococci and the need for efficient vaccines warrant further studies on the streptococcal molecules mediating complement resistance.

摘要

A组链球菌(GAS,化脓性链球菌)、B组链球菌(GBS,无乳链球菌)和肺炎链球菌都是人类病原体,在全球范围内导致了严重的发病和死亡。这些相关菌种会引发不同范围的感染,从轻微的上呼吸道或皮肤感染到败血症及重症疾病。为了引发深部感染并在人体内存活,细菌必须逃避免疫系统。补体是固有免疫的重要组成部分,既是一种调理和膜破坏级联反应,也是抗体的效应系统。在本综述中,我们描述了临床上最重要的三种链球菌菌种(A组和B组链球菌以及肺炎链球菌)的补体抗性机制。这三种菌种的补体逃避机制类似,但又彼此不同。所有这三种菌种的几个菌株都会表达一些分子(M蛋白、Bac或β、PspC),这些分子会将宿主液相补体调节因子H或C4b结合蛋白获取到其表面。A组和B组链球菌还会分泌蛋白质和/或酶,这些物质会抑制补体系统的激活或补体激活产物引起的趋化作用。尽管人们对链球菌的免疫逃避了解很多,但与链球菌感染相关的高发病率和死亡率以及对高效疫苗的需求,仍需要对介导补体抗性的链球菌分子进行进一步研究。

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