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回归热螺旋体,即回归热包柔氏螺旋体和达顿氏包柔氏螺旋体,可获得补体调节蛋白C4b结合蛋白和因子H。

Relapsing fever spirochetes Borrelia recurrentis and B. duttonii acquire complement regulators C4b-binding protein and factor H.

作者信息

Meri T, Cutler S J, Blom A M, Meri S, Jokiranta T S

机构信息

Haartman Institute, Department of Bacteriology and Immunology, P.O. Box 21, University of Helsinki, FIN-00014 Helsinki, Finland.

出版信息

Infect Immun. 2006 Jul;74(7):4157-63. doi: 10.1128/IAI.00007-06.

DOI:10.1128/IAI.00007-06
PMID:16790790
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1489703/
Abstract

Relapsing fever is a rapidly progressive and severe septic disease caused by certain Borrelia spirochetes. The disease is divided into two forms, i.e., epidemic relapsing fever, caused by Borrelia recurrentis and transmitted by lice, and the endemic form, caused by several Borrelia species, such as B. duttonii, and transmitted by soft-bodied ticks. The spirochetes enter the bloodstream by the vector bite and live persistently in plasma even after the development of specific antibodies. This leads to fever relapses and high mortality and clearly indicates that the Borrelia organisms utilize effective immune evasion strategies. In this study, we show that the epidemic relapsing fever pathogen B. recurrentis and an endemic relapsing fever pathogen, B. duttonii, are serum resistant, i.e., resistant to complement in vitro. They acquire the host alternative complement pathway regulator factor H on their surfaces in a similar way to that of the less serum-resistant Lyme disease pathogen, B. burgdorferi sensu stricto. More importantly, the relapsing fever spirochetes specifically bind host C4b-binding protein, a major regulator of the antibody-mediated classical complement pathway. Both complement regulators retained their functional activities when bound to the surfaces of the spirochetes. In conclusion, this is the first report of complement evasion by Borrelia recurrentis and B. duttonii and the first report showing capture of C4b-binding protein by spirochetes.

摘要

回归热是由某些疏螺旋体引起的一种迅速进展且严重的败血症性疾病。该疾病分为两种形式,即由回归热疏螺旋体引起、通过虱子传播的流行性回归热,以及由几种疏螺旋体(如达顿疏螺旋体)引起、通过软蜱传播的地方性回归热。螺旋体通过媒介叮咬进入血液,即使在特异性抗体产生后仍持续存在于血浆中。这导致发热复发和高死亡率,清楚地表明疏螺旋体利用了有效的免疫逃避策略。在本研究中,我们表明流行性回归热病原体回归热疏螺旋体和地方性回归热病原体达顿疏螺旋体具有血清抗性,即在体外对补体具有抗性。它们以与血清抗性较低的莱姆病病原体狭义伯氏疏螺旋体类似的方式在其表面获取宿主替代补体途径调节因子H。更重要的是,回归热螺旋体特异性结合宿主C4b结合蛋白,这是抗体介导的经典补体途径的主要调节因子。当这两种补体调节因子与螺旋体表面结合时,它们都保留了其功能活性。总之,这是关于回归热疏螺旋体和达顿疏螺旋体逃避补体的首次报道,也是螺旋体捕获C4b结合蛋白的首次报道。

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本文引用的文献

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Expression of complement factor H binding immunoevasion proteins in Borrelia garinii isolated from patients with neuroborreliosis.从神经莱姆病患者分离出的伽氏疏螺旋体中补体因子H结合免疫逃逸蛋白的表达
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The hyphal and yeast forms of Candida albicans bind the complement regulator C4b-binding protein.白色念珠菌的菌丝和酵母形式结合补体调节蛋白C4b结合蛋白。
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Identification and characterization of a linear-plasmid-encoded factor H-binding protein (FhbA) of the relapsing fever spirochete Borrelia hermsii.回归热螺旋体赫氏疏螺旋体线性质粒编码的因子H结合蛋白(FhbA)的鉴定与特性分析
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Generation of a complement-independent bactericidal IgM against a relapsing fever Borrelia.针对复发性发热疏螺旋体产生一种不依赖补体的杀菌性IgM。
J Immunol. 2004 Jan 15;172(2):1191-7. doi: 10.4049/jimmunol.172.2.1191.
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Complement resistance of Borrelia burgdorferi correlates with the expression of BbCRASP-1, a novel linear plasmid-encoded surface protein that interacts with human factor H and FHL-1 and is unrelated to Erp proteins.伯氏疏螺旋体的补体抗性与BbCRASP-1的表达相关,BbCRASP-1是一种新的线性质粒编码表面蛋白,它与人因子H和FHL-1相互作用,且与Erp蛋白无关。
J Biol Chem. 2004 Jan 23;279(4):2421-9. doi: 10.1074/jbc.M308343200. Epub 2003 Nov 7.
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Tick-borne relapsing fever caused by Borrelia hermsii, Montana.由赫氏疏螺旋体引起的蜱传回归热,蒙大拿州
Emerg Infect Dis. 2003 Sep;9(9):1151-4. doi: 10.3201/eid0909.030280.
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Analysis of the ability of spirochete species associated with relapsing fever, avian borreliosis, and epizootic bovine abortion to bind factor H and cleave c3b.分析与回归热、禽疏螺旋体病和牛流行性流产相关的螺旋体物种结合H因子和裂解C3b的能力。
J Clin Microbiol. 2003 Aug;41(8):3905-10. doi: 10.1128/JCM.41.8.3905-3910.2003.
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Complement inhibitor factor H binding to Lyme disease spirochetes is mediated by inducible expression of multiple plasmid-encoded outer surface protein E paralogs.补体抑制因子H与莱姆病螺旋体的结合是由多个质粒编码的外表面蛋白E旁系同源物的诱导表达介导的。
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The yeast Candida albicans binds complement regulators factor H and FHL-1.白色念珠菌可结合补体调节因子H和FHL-1。
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Infect Immun. 2002 Feb;70(2):491-7. doi: 10.1128/IAI.70.2.491-497.2002.