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莱姆病病原体伯氏疏螺旋体需要一种Dps同源物BB0690才能在蜱虫体内存活。

The Lyme disease agent Borrelia burgdorferi requires BB0690, a Dps homologue, to persist within ticks.

作者信息

Li Xin, Pal Utpal, Ramamoorthi Nandhini, Liu Xianzhong, Desrosiers Daniel C, Eggers Christian H, Anderson John F, Radolf Justin D, Fikrig Erol

机构信息

Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520-8031, USA.

出版信息

Mol Microbiol. 2007 Feb;63(3):694-710. doi: 10.1111/j.1365-2958.2006.05550.x. Epub 2006 Dec 20.

Abstract

Borrelia burgdorferi survives in an enzootic cycle, and Dps proteins protect DNA against damage during starvation or oxidative stress. The role of a Dps homologue encoded by Borrelia in spirochaete survival was assessed. Dps-deficient spirochaetes were infectious in mice via needle-inoculation at the dose of 10(5) spirochaetes. Larval ticks successfully acquired Dps-deficient spirochaetes via a blood meal on mice. However, after extended periods within unfed nymphs, the Dps-deficient spirochaetes failed to be transmitted to a new host when nymphs fed. Our data suggest that Dps functions to protect the spirochaetes during dormancy in unfed ticks, and in its absence, the spirochaetes become susceptible during tick feeding. dps is differentially expressed in vivo- low in mice and high in ticks - but constitutively expressed in vitro, showing little change during growth or in response to oxidative stress. Borrelia Dps forms a dodecameric complex capable of sequestering iron. The Dps-deficient spirochaetes showed no defect in starvation and oxidative stress assays, perhaps due to the lack of iron in spirochaetes grown in vitro. Dps is critical for spirochaete persistence within ticks, and strategies to interfere with Dps could potentially reduce Borrelia populations in nature and thereby influence the incidence of Lyme disease.

摘要

伯氏疏螺旋体在动物疫源循环中存活,而Dps蛋白在饥饿或氧化应激期间保护DNA免受损伤。评估了伯氏疏螺旋体编码的Dps同源物在螺旋体生存中的作用。Dps缺陷型螺旋体通过以10(5)个螺旋体的剂量进行针刺接种在小鼠中具有传染性。幼虫蜱通过吸食小鼠血液成功获取了Dps缺陷型螺旋体。然而,在未进食的若虫体内长时间停留后,当若虫进食时,Dps缺陷型螺旋体未能传播到新宿主。我们的数据表明,Dps在未进食蜱的休眠期间发挥作用以保护螺旋体,并且在其缺失时,螺旋体在蜱进食期间变得易感。dps在体内差异表达——在小鼠中低表达而在蜱中高表达——但在体外组成性表达,在生长过程中或对氧化应激反应时变化不大。伯氏疏螺旋体Dps形成能够螯合铁的十二聚体复合物。Dps缺陷型螺旋体在饥饿和氧化应激试验中未显示出缺陷,这可能是由于体外培养的螺旋体中缺乏铁。Dps对于螺旋体在蜱体内的持续存在至关重要,干扰Dps的策略可能会潜在地减少自然界中的伯氏疏螺旋体数量,从而影响莱姆病的发病率。

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