The classical complement pathway plays a critical role in the opsonisation of uropathogenic Escherichia coli

被引:22
作者
Li, Ke [1 ]
Sacks, Steven H. [1 ]
Sheerin, Neil S. [1 ,2 ]
机构
[1] Guys Hosp, Univ London Kings Coll, Dept Nephrol & Transplantat, London SE1 9RT, England
[2] Univ Newcastle Upon Tyne, Sch Clin Med Sci, Inst Cellular Med, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England
基金
英国惠康基金;
关键词
complement; Escherichia coli; urinary tract infection; innate immunity;
D O I
10.1016/j.molimm.2007.07.037
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Urinary tract infection due to uropathogenic Escherichia coli is a common clinical problem. The innate immune system and the uroepithelium are critical in defence against infection. The complement system is both part of the innate immune system and influences the interaction between epithelium and pathogen. We have therefore investigated the mechanism by which uropathogenic E. coli activate complement and the potential for this to occur during clinical infection. The classical pathway is responsible for bacterial opsonisation when complement proteins are present at low concentrations. At higher concentrations the alternative pathway predominates but still requires the classical pathway for its initiation. In contrast the mannose binding lectin pathway is not involved. Early classical pathway components are present in the urine during infection and actively contribute to bacterial opsonisation. The classical pathway could be initiated by anti-E. coli antibodies of IgG or IgM subclasses that are present in urine during infection. Additionally immunoglobulin-independent mechanisms, such as direct C1q binding to bacteria, may be involved. In conclusion, uropathogenic E. coli are readily opsonised by complement in a classical pathway dependent manner. This can occur within the urinary tract during the development of clinical infection. (c) 2007 Elsevier Ltd. All rights reserved.
引用
收藏
页码:954 / 962
页数:9
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