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首页> 外文期刊>Infection and immunity >Allelic Variation of the Lyme Disease Spirochete Adhesin DbpA Influences Spirochetal Binding to Decorin, Dermatan Sulfate, and Mammalian Cells
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Allelic Variation of the Lyme Disease Spirochete Adhesin DbpA Influences Spirochetal Binding to Decorin, Dermatan Sulfate, and Mammalian Cells

机译：莱姆病螺旋体黏附素DbpA的等位基因变异影响螺旋体与Decorin，硫酸皮肤素和哺乳动物细胞的结合。

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After transmission by an infected tick, the Lyme disease spirochete, Borrelia burgdorferi sensu lato, colonizes the mammalian skin and may disseminate systemically. The three major species of Lyme disease spirochete—B. burgdorferi sensu stricto, B. garinii, and B. afzelii—are associated with different chronic disease manifestations. Colonization is likely promoted by the ability to bind to target tissues, and Lyme disease spirochetes utilize multiple adhesive molecules to interact with diverse mammalian components. The allelic variable surface lipoprotein decorin binding protein A (DbpA) promotes bacterial binding to the proteoglycan decorin and to the glycosaminoglycan (GAG) dermatan sulfate. To assess allelic variation of DbpA in GAG-, decorin-, and cell-binding activities, we expressed dbpA alleles derived from diverse Lyme disease spirochetes in B. burgdorferi strain B314, a noninfectious and nonadherent strain that lacks dbpA. Each DbpA allele conferred upon B. burgdorferi strain B314 the ability to bind to cultured kidney epithelial (but not glial or endothelial) cells, as well as to purified decorin and dermatan sulfate. Nevertheless, allelic variation of DbpA was associated with dramatic differences in substrate binding activity. In most cases, decorin and dermatan sulfate binding correlated well, but DbpA of B. afzelii strain VS461 promoted differential binding to decorin and dermatan sulfate, indicating that the two activities are separable. DbpA from a clone of B. burgdorferi strain N40 that can cause disseminated infection in mice displayed relatively low adhesive activity, indicating that robust DbpA-mediated adhesive activity is not required for spread in the mammalian host.
机译：通过感染的tick传播后，莱姆病螺旋体（Borrelia burgdorferi sensu lato）定居在哺乳动物的皮肤上，可以全身传播。莱姆病螺旋体的三个主要种类-B。严格的burgdorferi sensu，B。garinii和B. afzelii与不同的慢性疾病表现有关。结合靶组织的能力可能促进定殖，而莱姆病螺旋体利用多种粘附分子与多种哺乳动物成分相互作用。等位基因可变表面脂蛋白核心蛋白聚糖结合蛋白A（DbpA）促进细菌与蛋白聚糖核心蛋白聚糖和糖胺聚糖（GAG）硫酸皮肤素的结合。为了评估GAG，除芯蛋白和细胞结合活性中DbpA的等位基因变异，我们在B. burgdorferi菌株B314中表达了来自各种莱姆病螺旋体的 dbpA 等位基因，该菌株缺乏感染性和非粘附性 dbpA 。每个DbpA等位基因赋予B. burgdorferi菌株B314结合培养的肾上皮（但不是神经胶质或内皮）细胞以及纯化的核心蛋白聚糖和硫酸皮肤素的能力。然而，DbpA的等位基因变异与底物结合活性的巨大差异有关。在大多数情况下，核心蛋白聚糖和硫酸皮肤素的结合相关性很好，但是非洲双歧杆菌VS461的DbpA促进了与核心蛋白聚糖和硫酸皮肤素的差异结合，表明这两种活性是可分离的。 B.burgdorferi菌株N40的克隆中的DbpA可能引起小鼠的弥漫性感染，表现出相对较低的黏附活性，这表明在哺乳动物宿主中传播不需要强大的DbpA介导的黏附活性。

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