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首页> 外文期刊>Infection and immunity >Host-Adapted Borrelia burgdorferi in Mice Expresses OspA during Inflammation
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Host-Adapted Borrelia burgdorferi in Mice Expresses OspA during Inflammation

机译：小鼠体内适应宿主的疏螺旋体伯氏疏螺旋体在炎症过程中表达OspA

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Antibody responses to outer surface protein A (OspA) of Borrelia burgdorferi may occur during periods of arthritis late in the clinical course of untreated Lyme disease. These antibody responses are paradoxical, given the conclusive evidence demonstrating that B. burgdorferi transmitted to the mammalian host expresses little or no OspA. The parallel occurrence of OspA antibodies and arthritic episodes suggests that OspA expression is upregulated during infection with B. burgdorferi. We hypothesized that this was due to the inflammatory environment caused by the immune response to the spirochete. To test our hypothesis, we adapted an in vivo model that mimics the host-pathogen interaction. Dialysis chambers containing B. burgdorferi were implanted into the peritoneal cavities of mice in the presence or absence of zymosan, a yeast cell wall extract that induces inflammation. Spirochetes were harvested 2 days later, and OspA expression was assessed at the protein and transcription level by Western blotting and real-time reverse transcription-PCR, respectively. Flow cytometry was also utilized to evaluate OspA protein expression on individual spirochetes. B. burgdorferi maintained in an inflammatory in vivo environment show an increased OspA expression relative to B. burgdorferi kept under normal in vivo conditions. Furthermore, host-adapted B. burgdorferi with a low OspA phenotype upregulates OspA expression when transferred to an inflammatory in vivo environment. The results obtained by these techniques uniformly identify inflammation as a mediator of in vivo OspA expression in host-adapted B. burgdorferi, providing insights into the behavior of live spirochetes in the mammalian host.
机译：在未经治疗的莱姆病的临床病程中，关节炎期间可能会发生对伯氏疏螺旋体外表面蛋白A（OspA）的抗体反应。考虑到证明 B的确凿证据，这些抗体反应是自相矛盾的。传播给哺乳动物宿主的burgdorferi 很少或不表达OspA。 OspA抗体和关节炎发作的并行发生表明在 B感染期间OspA表达被上调。 burgdorferi 。我们假设这是由于对螺旋体的免疫反应引起的炎性环境。为了检验我们的假设，我们采用了模拟宿主与病原体相互作用的体内模型。含有 B的透析室。在存在或不存在zymosan（一种诱导炎症的酵母细胞壁提取物）的情况下，将burgdorferi 植入小鼠的腹腔。 2天后收获螺旋体，分别通过蛋白质印迹和实时逆转录-PCR在蛋白和转录水平上评估OspA表达。流式细胞仪还用于评估单个螺旋体上OspA蛋白的表达。 B。相对于 B，维持在炎性体内环境中的burgdorferi 显示OspA表达增加。 burgdorferi 保持在正常的体内条件下。此外，适应宿主的 B。 OspA表型低的burgdorferi 在转移到体内炎症环境后会上调OspA表达。通过这些技术获得的结果一致地确定炎症为宿主适应性 B中体内OspA表达的介质。 burgdorferi ，提供有关哺乳动物宿主中活螺旋体行为的见解。

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