Li Xin, Neelakanta Girish, Liu Xianzhong, Beck Deborah S, Kantor Fred S, Fish Durland, Anderson John F, Fikrig Erol
Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, 300 Cedar Street, New Haven, CT 06520-8031, USA.
Infect Immun. 2007 Sep;75(9):4237-44. doi: 10.1128/IAI.00632-07. Epub 2007 Jul 9.
Borrelia burgdorferi preferentially induces selected genes in mice or ticks, and studies suggest that ospD is down-regulated in response to host-specific signals. We now directly show that ospD expression is generally elevated within Ixodes scapularis compared with mice. We then assessed the importance of OspD throughout the spirochete life cycle by generating OspD-deficient B. burgdorferi and examining the mutant in the murine model of tick-transmitted Lyme borreliosis. The lack of OspD did not influence B. burgdorferi infectivity in mice or the acquisition of spirochetes by I. scapularis. OspD adhered to tick gut extracts in vitro, and the OspD-deficient B. burgdorferi strain had a threefold decrease in colonization of the tick gut in vivo. This decrease, however, did not alter subsequent spirochete transmission during a second blood meal. These data suggest that B. burgdorferi can compensate for the lack of OspD in both ticks and mice and that OspD may have a nonessential, secondary, role in B. burgdorferi persistence within I. scapularis.
伯氏疏螺旋体优先诱导小鼠或蜱中的特定基因,研究表明ospD会响应宿主特异性信号而下调。我们现在直接表明,与小鼠相比,肩突硬蜱体内的ospD表达普遍升高。然后,我们通过构建ospD缺陷型伯氏疏螺旋体并在蜱传播莱姆病疏螺旋体病的小鼠模型中检查该突变体,评估了OspD在整个螺旋体生命周期中的重要性。缺乏OspD并不影响伯氏疏螺旋体在小鼠中的感染性或肩突硬蜱获取螺旋体的能力。OspD在体外可粘附于蜱肠道提取物,且ospD缺陷型伯氏疏螺旋体菌株在体内蜱肠道定殖能力下降了三倍。然而,这种下降并未改变在第二次吸血期间随后的螺旋体传播。这些数据表明,伯氏疏螺旋体可以弥补蜱和小鼠中OspD的缺乏,并且OspD可能在伯氏疏螺旋体在肩突硬蜱体内的持续存在中具有非必需的次要作用。