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首页> 外文期刊>Infection and immunity >Borrelia burgdorferi Harbors a Transport System Essential for Purine Salvage and Mammalian Infection
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Borrelia burgdorferi Harbors a Transport System Essential for Purine Salvage and Mammalian Infection

机译：伯氏疏螺旋体（Borrelia burgdorferi）具有嘌呤打捞和哺乳动物感染必不可少的运输系统

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Borrelia burgdorferi is the tick-borne bacterium that causes the multistage inflammatory disease Lyme disease. B. burgdorferi has a reduced genome and lacks the enzymes required for de novo synthesis of purines for synthesis of RNA and DNA. Therefore, this obligate pathogen is dependent upon the tick vector and mammalian host environments for salvage of purine bases for nucleic acid biosynthesis. This pathway is vital for B. burgdorferi survival throughout its infectious cycle, as key enzymes in the purine salvage pathway are essential for the ability of the spirochete to infect mice and critical for spirochete replication in the tick. The transport of preformed purines into the spirochete is the first step in the purine salvage pathway and may represent a novel therapeutic target and/or means to deliver antispirochete molecules to the pathogen. However, the transport systems critical for purine salvage by B. burgdorferi have yet to be identified. Herein, we demonstrate that the genes bbb22 and bbb23, present on B. burgdorferi's essential plasmid circular plasmid 26 (cp26), encode key purine transport proteins. BBB22 and/or BBB23 is essential for hypoxanthine transport and contributes to the transport of adenine and guanine. Furthermore, B. burgdorferi lacking bbb22-23 was noninfectious in mice up to a dose of 1 × 107 spirochetes. Together, our data establish that bbb22-23 encode purine permeases critical for B. burgdorferi mammalian infectivity, suggesting that this transport system may serve as a novel antimicrobial target for the treatment of Lyme disease.
机译：伯氏疏螺旋体（Borrelia burgdorferi）是由tick传播的细菌，引起多阶段炎性疾病莱姆病。 B. burgdorferi基因组减少，缺乏从头合成新嘌呤以合成RNA和DNA所需的酶。因此，该专性病原体依赖壁虱载体和哺乳动物宿主环境来挽救嘌呤碱基以进行核酸生物合成。由于嘌呤挽救途径中的关键酶对于螺旋体感染小鼠的能力是必不可少的，并且对于壁虱在壁虱中的复制至关重要，因此该途径对于整个伯氏疏螺旋体的生存至关重要。预先形成的嘌呤向螺旋体的转运是嘌呤挽救途径的第一步，可能代表了一种新颖的治疗靶标和/或将抗螺体化学分子递送至病原体的手段。然而，尚需鉴定对伯氏疏螺旋体挽救嘌呤至关重要的运输系统。本文中，我们证明了存在于伯氏疏螺旋体必需质粒环状质粒26（cp26）上的基因 bbb22 和 bbb23 编码关键的嘌呤转运蛋白。 BBB22和/或BBB23对于次黄嘌呤的运输至关重要，并有助于腺嘌呤和鸟嘌呤的运输。此外，缺乏 bbb22-23 的B. burgdorferi在小鼠中无感染性，剂量高达1×10 7 螺旋。在一起，我们的数据确定 bbb22-23 编码对B. burgdorferi哺乳动物的感染至关重要的嘌呤通透酶，表明该转运系统可以作为治疗莱姆病的新型抗菌靶标。

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