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Gliding Motility Leads to Active Cellular Invasion by Cryptosporidium parvum Sporozoites

机译:滑行运动导致小隐孢子虫子孢子活跃的细胞入侵。

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摘要

We examined gliding motility and cell invasion by an early-branching apicomplexan, Cryptosporidium parvum, which causes diarrheal disease in humans and animals. Real-time video microscopy demonstrated that C. parvum sporozoites undergo circular and helical gliding, two of the three stereotypical movements exhibited by Toxoplasma gondii tachyzoites. C. parvum sporozoites moved more rapidly than T. gondii sporozoites, which showed the same rates of motility as tachyzoites. Motility by C. parvum sporozoites was prevented by latrunculin B and cytochalasin D, drugs that depolymerize the parasite actin cytoskeleton, and by the myosin inhibitor 2,3-butanedione monoxime. Imaging of the initial events in cell entry by Cryptosporidium revealed that invasion occurs rapidly; however, the parasite does not enter deep into the cytosol but rather remains at the cell surface in a membrane-bound compartment. Invasion did not stimulate rearrangement of the host cell cytoskeleton and was inhibited by cytochalasin D, even in host cells that were resistant to the drug. Our studies demonstrate that C. parvum relies on a conserved actin-myosin motor for motility and active penetration of its host cell, thus establishing that this is a widely conserved feature of the Apicomplexa.
机译:我们研究了由早期分支的apicomplexan隐孢子虫小孢子(Cryptosporidium parvum)引起的滑行运动和细胞侵袭,它引起人和动物的腹泻病。实时视频显微镜显示,小球藻孢子体经历圆形和螺旋滑动,这是弓形虫速殖子表现出的三个定型运动中的两个。 C. parvum子孢子的移动速度比刚地弓形虫的子孢子快,后者的运动速度与速殖子相同。 latrunculin B和cytochalasin D,使寄生虫肌动蛋白细胞骨架解聚的药物以及肌球蛋白抑制剂2,3-丁二酮单肟阻止了C. parvum子孢子的运动。隐孢子虫对细胞进入的初始事件的成像显示,侵袭迅速发生。然而,该寄生虫不会进入细胞质的深处,而是保留在膜结合区室的细胞表面。侵袭不刺激宿主细胞骨架的重排,并且甚至在对药物有抗性的宿主细胞中也被细胞松弛素D抑制。我们的研究表明,小球藻依赖于保守的肌动蛋白-肌球蛋白运动来促进其宿主细胞的运动和主动渗透,因此证明这是蚜虫复合体的一个广泛保守的特征。

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