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本文引用的文献

1
Borrelia burgdorferi locus BB0795 encodes a BamA orthologue required for growth and efficient localization of outer membrane proteins.伯氏疏螺旋体 BB0795 基因座编码 BamA 同源物,该同源物对于生长和外膜蛋白的有效定位是必需的。
Mol Microbiol. 2010 Feb;75(3):692-709. doi: 10.1111/j.1365-2958.2009.07015.x. Epub 2009 Dec 16.
2
CspA-mediated binding of human factor H inhibits complement deposition and confers serum resistance in Borrelia burgdorferi.CspA介导的人补体因子H的结合可抑制补体沉积,并赋予伯氏疏螺旋体血清抗性。
Infect Immun. 2009 Jul;77(7):2773-82. doi: 10.1128/IAI.00318-09. Epub 2009 May 18.
3
Borrelia burgdorferi infection-associated surface proteins ErpP, ErpA, and ErpC bind human plasminogen.伯氏疏螺旋体感染相关表面蛋白ErpP、ErpA和ErpC可结合人纤溶酶原。
Infect Immun. 2009 Jan;77(1):300-6. doi: 10.1128/IAI.01133-08. Epub 2008 Nov 10.
4
Borrelia burgdorferi complement regulator-acquiring surface protein 2 does not contribute to complement resistance or host infectivity.伯氏疏螺旋体补体调节蛋白获取表面蛋白2对补体抗性或宿主感染性无作用。
PLoS One. 2008 Aug 20;3(8):3010e. doi: 10.1371/journal.pone.0003010.
5
Coordinated expression of Borrelia burgdorferi complement regulator-acquiring surface proteins during the Lyme disease spirochete's mammal-tick infection cycle.伯氏疏螺旋体补体调节蛋白获取表面蛋白在莱姆病螺旋体哺乳动物-蜱感染周期中的协同表达。
Infect Immun. 2007 Sep;75(9):4227-36. doi: 10.1128/IAI.00604-07. Epub 2007 Jun 11.
6
Rapid clearance of Lyme disease spirochetes lacking OspC from skin.皮肤中缺乏外膜蛋白C(OspC)的莱姆病螺旋体的快速清除。
Infect Immun. 2007 Mar;75(3):1517-9. doi: 10.1128/IAI.01725-06. Epub 2006 Dec 11.
7
Functional characterization of BbCRASP-2, a distinct outer membrane protein of Borrelia burgdorferi that binds host complement regulators factor H and FHL-1.BbCRASP-2的功能特性,BbCRASP-2是伯氏疏螺旋体一种独特的外膜蛋白,可结合宿主补体调节因子H和FHL-1。
Mol Microbiol. 2006 Sep;61(5):1220-36. doi: 10.1111/j.1365-2958.2006.05318.x.
8
Evidence that the BBA68 protein (BbCRASP-1) of the Lyme disease spirochetes does not contribute to factor H-mediated immune evasion in humans and other animals.有证据表明,莱姆病螺旋体的BBA68蛋白(BbCRASP-1)对人类和其他动物中因子H介导的免疫逃逸没有作用。
Infect Immun. 2006 May;74(5):3030-4. doi: 10.1128/IAI.74.5.3030-3034.2006.
9
Complement regulator-acquiring surface protein 1 imparts resistance to human serum in Borrelia burgdorferi.补体调节蛋白获取表面蛋白1赋予伯氏疏螺旋体对人血清的抗性。
J Immunol. 2005 Sep 1;175(5):3299-308. doi: 10.4049/jimmunol.175.5.3299.
10
Combined effects of blood and temperature shift on Borrelia burgdorferi gene expression as determined by whole genome DNA array.通过全基因组DNA芯片确定血液和温度变化对伯氏疏螺旋体基因表达的联合影响。
Infect Immun. 2004 Sep;72(9):5419-32. doi: 10.1128/IAI.72.9.5419-5432.2004.

OspE 相关蛋白抑制补体沉积并增强莱姆病螺旋体伯氏疏螺旋体的血清抗性。

The OspE-related proteins inhibit complement deposition and enhance serum resistance of Borrelia burgdorferi, the lyme disease spirochete.

机构信息

Department of Microbiology and Immunology, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.

出版信息

Infect Immun. 2011 Apr;79(4):1451-7. doi: 10.1128/IAI.01274-10. Epub 2011 Jan 31.

DOI:10.1128/IAI.01274-10
PMID:21282413
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3067540/
Abstract

Borrelia burgdorferi, the Lyme disease spirochete, binds the host complement inhibitors factor H (FH) and FH-like protein 1 (FHL-1). Binding of FH/FHL-1 by the B. burgdorferi proteins CspA and the OspE-related proteins is thought to enhance resistance to serum-mediated killing. While previous reports have shown that CspA confers serum resistance in B. burgdorferi, it is unclear whether the OspE-related proteins are relevant in B. burgdorferi serum resistance when OspE is expressed on the borrelial surface. To assess the role of the OspE-related proteins, we overexpressed them in a serum-sensitive CspA mutant strain. OspE overexpression enhanced serum resistance of the CspA-deficient organisms. Furthermore, FH was more efficiently bound to the B. burgdorferi surface when OspE was overexpressed. Deposition of complement components C3 and C5b-9 (the membrane attack complex), however, was reduced on the surface of the OspE-overexpressing strain compared to that on the CspA mutant strain. These data demonstrate that OspE proteins expressed on the surface of B. burgdorferi bind FH and protect the organism from complement deposition and subsequent serum-mediated destruction.

摘要

伯氏疏螺旋体,莱姆病螺旋体,可结合宿主补体抑制剂因子 H(FH)和 FH 样蛋白 1(FHL-1)。据认为,B. burgdorferi 蛋白 CspA 和 OspE 相关蛋白与 FH/FHL-1 的结合增强了对血清介导杀伤的抵抗力。尽管先前的报告表明 CspA 可赋予 B. burgdorferi 血清抗性,但当 OspE 表达于螺旋体表面时,OspE 相关蛋白是否与 B. burgdorferi 血清抗性相关尚不清楚。为了评估 OspE 相关蛋白的作用,我们在血清敏感的 CspA 突变株中过表达了它们。OspE 的过表达增强了 CspA 缺陷生物的血清抗性。此外,当 OspE 过表达时,FH 更有效地结合到 B. burgdorferi 表面。然而,与 CspA 突变株相比,OspE 过表达株表面补体成分 C3 和 C5b-9(膜攻击复合物)的沉积减少。这些数据表明,表达在 B. burgdorferi 表面的 OspE 蛋白结合 FH,保护生物体免受补体沉积和随后的血清介导的破坏。