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本文引用的文献

1
Complement regulator-acquiring surface protein 1 of Borrelia burgdorferi binds to human bone morphogenic protein 2, several extracellular matrix proteins, and plasminogen.伯氏疏螺旋体补体调控蛋白获取表面蛋白 1 与人骨形态发生蛋白 2、几种细胞外基质蛋白和纤溶酶原结合。
J Infect Dis. 2010 Aug 15;202(3):490-8. doi: 10.1086/653825.
2
Central role of the Holliday junction helicase RuvAB in vlsE recombination and infectivity of Borrelia burgdorferi.RuvAB 解旋酶在伯氏疏螺旋体 vlsE 重组和感染中的中心作用。
PLoS Pathog. 2009 Dec;5(12):e1000679. doi: 10.1371/journal.ppat.1000679. Epub 2009 Dec 4.
3
Investigation of the genes involved in antigenic switching at the vlsE locus in Borrelia burgdorferi: an essential role for the RuvAB branch migrase.研究伯氏疏螺旋体 vlsE 基因座抗原转换相关基因:RuvAB 分支迁移酶的重要作用。
PLoS Pathog. 2009 Dec;5(12):e1000680. doi: 10.1371/journal.ppat.1000680. Epub 2009 Dec 4.
4
Borrelia burgdorferi BmpA is a laminin-binding protein.伯氏疏螺旋体BmpA是一种层粘连蛋白结合蛋白。
Infect Immun. 2009 Nov;77(11):4940-6. doi: 10.1128/IAI.01420-08. Epub 2009 Aug 24.
5
A novel fibronectin binding motif in MSCRAMMs targets F3 modules.微生物表面成分识别黏附分子(MSCRAMMs)中一种新型纤连蛋白结合基序靶向F3结构域。
PLoS One. 2009;4(4):e5412. doi: 10.1371/journal.pone.0005412. Epub 2009 Apr 30.
6
Borrelia burgdorferi RevA antigen binds host fibronectin.伯氏疏螺旋体RevA抗原与宿主纤连蛋白结合。
Infect Immun. 2009 Jul;77(7):2802-12. doi: 10.1128/IAI.00227-09. Epub 2009 Apr 27.
7
A chromosomally encoded virulence factor protects the Lyme disease pathogen against host-adaptive immunity.一种染色体编码的毒力因子可保护莱姆病病原体免受宿主适应性免疫的影响。
PLoS Pathog. 2009 Mar;5(3):e1000326. doi: 10.1371/journal.ppat.1000326. Epub 2009 Mar 6.
8
The Borrelia burgdorferi outer-surface protein ErpX binds mammalian laminin.伯氏疏螺旋体外表面蛋白ErpX可结合哺乳动物层粘连蛋白。
Microbiology (Reading). 2009 Mar;155(Pt 3):863-872. doi: 10.1099/mic.0.024604-0.
9
Detection and quantification of Lyme spirochetes using sensitive and specific molecular beacon probes.使用灵敏且特异的分子信标探针检测和定量莱姆螺旋体。
BMC Microbiol. 2009 Feb 24;9:43. doi: 10.1186/1471-2180-9-43.
10
Complement activation and inhibition: a delicate balance.补体激活与抑制:微妙的平衡。
Trends Immunol. 2009 Feb;30(2):83-90. doi: 10.1016/j.it.2008.11.003. Epub 2009 Jan 12.

伯氏疏螺旋体的黏附机制。

Adhesion mechanisms of Borrelia burgdorferi.

机构信息

Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, MA, USA.

出版信息

Adv Exp Med Biol. 2011;715:35-49. doi: 10.1007/978-94-007-0940-9_3.

DOI:10.1007/978-94-007-0940-9_3
PMID:21557056
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4521209/
Abstract

The Borrelia are widely distributed agents of Lyme disease and Relapsing Fever. All are vector-borne zoonotic pathogens, have segmented genomes, and enigmatic mechanisms of pathogenesis. Adhesion to mammalian and tick substrates is one pathogenic mechanism that has been widely studied. At this point, the primary focus of research in this area has been on Borrelia burgdorferi, one agent of Lyme disease, but many of the adhesins of B. burgdorferi are conserved in other Lyme disease agents, and some are conserved in the Relapsing Fever Borrelia. B. burgdorferi adhesins that mediate attachment to cell-surface molecules may influence the host response to the bacteria, while adhesins that mediate attachment to soluble proteins or extracellular matrix components may cloak the bacterial surface from recognition by the host immune system as well as facilitate colonization of tissues. While targeted mutations in the genes encoding some adhesins have been shown to affect the infectivity and pathogenicity of B. burgdorferi, much work remains to be done to understand the roles of the adhesins in promoting the persistent infection required to maintain the bacteria in reservoir hosts.

摘要

伯氏疏螺旋体是莱姆病和回归热的广泛分布的病原体。所有这些病原体都是通过媒介传播的动物源性人畜共患病病原体,具有节段性基因组和神秘的发病机制。黏附哺乳动物和蜱类宿主是一种广泛研究的发病机制。在这一领域,目前的研究重点主要集中在莱姆病的一种病原体伯氏疏螺旋体上,但伯氏疏螺旋体的许多黏附素在其他莱姆病病原体中是保守的,有些在回归热螺旋体中也是保守的。伯氏疏螺旋体黏附素介导与细胞表面分子的附着,可能会影响宿主对细菌的反应,而介导与可溶性蛋白或细胞外基质成分附着的黏附素可以掩盖细菌表面,使其免受宿主免疫系统的识别,并有助于在组织中定植。虽然靶向突变编码某些黏附素的基因已被证明会影响伯氏疏螺旋体的感染力和致病性,但仍有许多工作需要做,以了解黏附素在促进持续感染方面的作用,以维持细菌在储存宿主中的存在。