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The Lyme disease agent exploits a tick protein to infect the mammalian host

机译:莱姆病病原体利用a蛋白感染哺乳动物宿主

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The Lyme disease agent, Borrelia burgdorferi, is maintained in a tick-mouse cycle. Here we show that B. burgdorferi usurps a tick salivary protein, Salp15 (ref. 3), to facilitate the infection of mice. The level of salp15 expression was selectively enhanced by the presence of B. burgdorferi in Ixodes scapularis, first indicating that spirochaetes might use Salp15 during transmission. Salp15 was then shown to adhere to the spirochaete, both in vitro and in vivo, and specifically interacted with B. burgdorferi outer surface protein C. The binding of Salpl5 protected B. burgdorferi from antibody-mediated killing in vitro and provided spirochaetes with a marked advantage when they were inoculated into naive mice or animals previously infected with B. burgdorferi. Moreover, RNA interference-mediated repression of salp 15 in I. scapularis drastically reduced the capacity of tick-borne spirochaetes to infect mice. These results show the capacity of a pathogen to use a secreted arthropod protein to help it colonize the mammalian host.
机译:莱姆病病原体伯氏疏螺旋体(Borrelia burgdorferi)处于a鼠周期。在这里,我们显示B. burgdorferi篡夺了唾液唾液蛋白Salp15(参考文献3),以促进小鼠的感染。 Salp15的表达水平被肩x小体中的B. burgdorferi选择性地增强,首先表明螺旋体可能在传播过程中使用Salp15。然后显示Salp15在体外和体内均能粘附到螺旋线虫上,并与B. burgdorferi外表面蛋白C发生特异性相互作用。Salpl5的结合可保护B. burgdorferi免受抗体介导的体外杀灭作用,并为spirochaetes提供了明显的当将它们接种到幼稚小鼠或先前感染过伯氏疏螺旋体的动物中时,它们的优势。此外,在肩mediated肉中RNA干扰介导的抑制salp 15大大降低了tick传螺旋体感染小鼠的能力。这些结果表明,病原体利用分泌的节肢动物蛋白帮助其定居哺乳动物宿主的能力。

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