An Ixodes scapularis Protein Disulfide Isomerase Contributes to Borrelia burgdorferi Colonization of the Vector.
An Ixodes scapularis Protein Disulfide Isomerase Contributes to Borrelia burgdorferi Colonization of the Vector.
复制标题
肩胛硬蜱蛋白质二硫键异构酶对伯氏疏螺旋体在载体中的定殖有贡献。
DOI：
10.1128/iai.00426-20
复制
发表时间：
2020-11-16
影响因子：
3.1
通讯作者：
Fikrig E
中科院分区：
文献类型：
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作者：
Cao Y;Rosen C;Arora G;Gupta A;Booth CJ;Murfin KE;Cerny J;Marin Lopez A;Chuang YM;Tang X;Pal U;Ring A;Narasimhan S;Fikrig E
伯氏疏螺旋体导致莱姆病，这是北美最常见的蜱传播疾病。当肩突硬蜱以受感染的脊椎动物宿主为食时，螺旋体随血粉沿着进入蜱肠道并在载体上定殖。在这里，我们表明，分泌的蜱蛋白，我。肩胛肌蛋白二硫键异构酶A3（IsPDIA 3），增强B。蜱肠道的伯氏菌定植。伯氏疏螺旋体导致莱姆病，这是北美最常见的蜱传播疾病。当肩突硬蜱以受感染的脊椎动物宿主为食时，螺旋体随血粉沿着进入蜱肠道并在载体上定殖。在这里，我们表明，分泌的蜱蛋白，我。肩胛肌蛋白二硫键异构酶A3（IsPDIA 3），增强B。蜱肠道的伯氏菌定植。I.其中ispdiA 3已使用RNA干扰敲低的肩胛蜱在饱食B后减少了蜱肠道的螺旋体定殖。感染伯氏菌的小鼠。此外，施用针对B的IsPDIA 3抗血清。感染伯氏螺旋体的小鼠在进食这些动物时降低了螺旋体在蜱虫上定殖的能力。我们发现，IsPDIA 3调节蜱叮咬部位的炎症反应，可能促进螺旋体在载体-宿主界面的存活，因为它退出脊椎动物宿主进入蜱肠道。这些数据提供了对B之间复杂相互作用的功能性见解。burgdorferi及其节肢动物载体，并提出了干扰螺旋体生命周期的其他靶标。
Borrelia burgdorferi causes Lyme disease, the most common tick-transmitted illness in North America. When Ixodes scapularis feed on an infected vertebrate host, spirochetes enter the tick gut along with the bloodmeal and colonize the vector. Here, we show that a secreted tick protein, I. scapularis protein disulfide isomerase A3 (IsPDIA3), enhances B. burgdorferi colonization of the tick gut. Borrelia burgdorferi causes Lyme disease, the most common tick-transmitted illness in North America. When Ixodes scapularis feed on an infected vertebrate host, spirochetes enter the tick gut along with the bloodmeal and colonize the vector. Here, we show that a secreted tick protein, I. scapularis protein disulfide isomerase A3 (IsPDIA3), enhances B. burgdorferi colonization of the tick gut. I. scapularis ticks in which ispdiA3 has been knocked down using RNA interference have decreased spirochete colonization of the tick gut after engorging on B. burgdorferi-infected mice. Moreover, administration of IsPDIA3 antiserum to B. burgdorferi-infected mice reduced the ability of spirochetes to colonize the tick when feeding on these animals. We show that IsPDIA3 modulates inflammatory responses at the tick bite site, potentially facilitating spirochete survival at the vector-host interface as it exits the vertebrate host to enter the tick gut. These data provide functional insights into the complex interactions between B. burgdorferi and its arthropod vector and suggest additional targets to interfere with the spirochete life cycle.