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伯氏疏螺旋体通过外膜蛋白 C 促进特异性关节侵袭和定殖。

Strain-specific joint invasion and colonization by Lyme disease spirochetes is promoted by outer surface protein C.

机构信息

Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts, United States of America.

Division of Infectious Diseases, New York State Department of Health, Wadsworth Center, Albany, New York, United States of America.

出版信息

PLoS Pathog. 2020 May 15;16(5):e1008516. doi: 10.1371/journal.ppat.1008516. eCollection 2020 May.

Abstract

Lyme disease, caused by Borrelia burgdorferi, B. afzelii and B. garinii, is a chronic, multi-systemic infection and the spectrum of tissues affected can vary with the Lyme disease strain. For example, whereas B. garinii infection is associated with neurologic manifestations, B. burgdorferi infection is associated with arthritis. The basis for tissue tropism is poorly understood, but has been long hypothesized to involve strain-specific interactions with host components in the target tissue. OspC (outer surface protein C) is a highly variable outer surface protein required for infectivity, and sequence differences in OspC are associated with variation in tissue invasiveness, but whether OspC directly influences tropism is unknown. We found that OspC binds to the extracellular matrix (ECM) components fibronectin and/or dermatan sulfate in an OspC variant-dependent manner. Murine infection by isogenic B. burgdorferi strains differing only in their ospC coding region revealed that two OspC variants capable of binding dermatan sulfate promoted colonization of all tissues tested, including joints. However, an isogenic strain producing OspC from B. garinii strain PBr, which binds fibronectin but not dermatan sulfate, colonized the skin, heart and bladder, but not joints. Moreover, a strain producing an OspC altered to recognize neither fibronectin nor dermatan sulfate displayed dramatically reduced levels of tissue colonization that were indistinguishable from a strain entirely deficient in OspC. Finally, intravital microscopy revealed that this OspC mutant, in contrast to a strain producing wild type OspC, was defective in promoting joint invasion by B. burgdorferi in living mice. We conclude that OspC functions as an ECM-binding adhesin that is required for joint invasion, and that variation in OspC sequence contributes to strain-specific differences in tissue tropism displayed among Lyme disease spirochetes.

摘要

莱姆病是由伯氏疏螺旋体、阿弗西尼亚疏螺旋体和伽氏疏螺旋体引起的慢性、全身性感染,受感染的组织范围可能因莱姆病菌株的不同而有所差异。例如,感染伽氏疏螺旋体与神经系统表现有关,而感染伯氏疏螺旋体与关节炎有关。组织嗜性的基础尚不清楚,但长期以来一直假设与宿主组织中特定菌株的相互作用有关。OspC(外膜蛋白 C)是一种高度可变的外膜蛋白,对于感染性是必需的,OspC 序列的差异与组织侵袭性的变化有关,但 OspC 是否直接影响嗜性尚不清楚。我们发现 OspC 以 OspC 变异体依赖的方式结合细胞外基质(ECM)成分纤连蛋白和/或硫酸皮肤素。通过仅在 ospC 编码区存在差异的同源伯氏疏螺旋体菌株进行的小鼠感染实验表明,两种能够结合硫酸皮肤素的 OspC 变体促进了所有测试组织的定植,包括关节。然而,一种产生源自伯氏疏螺旋体 PBr 菌株的 OspC 的同源菌株,该 OspC 能够结合纤连蛋白但不能结合硫酸皮肤素,仅定植于皮肤、心脏和膀胱,而不能定植于关节。此外,一种产生既不能识别纤连蛋白也不能识别硫酸皮肤素的 OspC 变体的菌株,其组织定植水平显著降低,与完全缺乏 OspC 的菌株无明显差异。最后,活体显微镜观察显示,与产生野生型 OspC 的菌株相比,这种 OspC 突变体在促进活鼠体内伯氏疏螺旋体入侵关节方面存在缺陷。我们得出结论,OspC 作为一种 ECM 结合黏附素发挥作用,是关节入侵所必需的,而 OspC 序列的差异导致莱姆病螺旋体之间表现出特定菌株的组织嗜性差异。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/114d/7255614/02fd31728a95/ppat.1008516.g001.jpg

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