Division of Infectious Diseases, Wadsworth Center, New York State Department of Health, Albany, NY, USA; Department of Biomedical Sciences, SUNY University at Albany, Albany, NY, USA.
Division of Infectious Diseases, Wadsworth Center, New York State Department of Health, Albany, NY, USA.
Ticks Tick Borne Dis. 2023 Jan;14(1):102081. doi: 10.1016/j.ttbdis.2022.102081. Epub 2022 Nov 10.
In North America, Lyme disease is primarily caused by the spirochetal bacterium Borrelia burgdorferi sensu stricto (Bb), which is transmitted between multiple vertebrate hosts and ixodid ticks, and is a model commonly used to study host-pathogen interactions. While Bb is consistently observed in its mammalian and avian reservoirs, the bacterium is rarely isolated from North American reptiles. Two closely related lizard species, the eastern fence lizard (Sceloporus undulatus) and the western fence lizard (Sceloporus occidentalis), are examples of reptiles parasitized by Ixodes ticks. Vertebrates are known to generate complement as an innate defense mechanism, which can be activated before Bb disseminate to distal tissues. Complement from western fence lizards has proven lethal against one Bb strain, implying the role of complement in making those lizards unable to serve as hosts to Bb. However, Bb DNA is occasionally identified in distal tissues of field-collected eastern fence lizards, suggesting some Bb strains may overcome complement-mediated clearance in these lizards. These findings raise questions regarding the role of complement and its impact on Bb interactions with North American lizards. In this study, we found Bb seropositivity in a small population of wild-caught eastern fence lizards and observed Bb strain-specific survivability in lizard sera. We also found that a Bb outer surface protein, OspE, from Bb strains viable in sera, promotes lizard serum survivability and binds to a complement inhibitor, factor H, from eastern fence lizards. Our data thus identify bacterial and host determinants of eastern fence lizard complement evasion, providing insights into the role of complement influencing Bb interactions with North American lizards.
在北美，莱姆病主要由螺旋体细菌伯氏疏螺旋体严格意义上（Bb）引起，该细菌在多种脊椎动物宿主和硬蜱之间传播，是研究宿主-病原体相互作用的常用模型。虽然 Bb 在其哺乳动物和鸟类宿主中始终存在，但很少从北美的爬行动物中分离出该细菌。两种密切相关的蜥蜴物种，东部栅栏蜥蜴（Sceloporus undulatus）和西部栅栏蜥蜴（Sceloporus occidentalis），是被Ixodes 蜱寄生的爬行动物的例子。众所周知，脊椎动物会产生补体作为先天防御机制，该机制可以在 Bb 传播到远处组织之前被激活。来自西部栅栏蜥蜴的补体已被证明对一种 Bb 菌株具有致命性，这意味着补体在使这些蜥蜴无法成为 Bb 的宿主方面发挥作用。然而，偶尔会在野外采集的东部栅栏蜥蜴的远处组织中鉴定出 Bb DNA，这表明某些 Bb 菌株可能会克服补体介导的清除作用。这些发现提出了有关补体的作用及其对 Bb 与北美的蜥蜴相互作用的影响的问题。在这项研究中，我们在一小部分野生捕获的东部栅栏蜥蜴中发现了 Bb 血清阳性，并观察到蜥蜴血清中 Bb 菌株特异性存活率。我们还发现，来自在血清中存活的 Bb 菌株的 Bb 外表面蛋白 OspE 促进了蜥蜴血清的存活，并与来自东部栅栏蜥蜴的补体抑制剂因子 H 结合。因此，我们的数据确定了东部栅栏蜥蜴补体逃避的细菌和宿主决定因素，为补体影响 Bb 与北美的蜥蜴相互作用的作用提供了线索。
