Mechanisms of Chlamydia trachomatis entry into nonphagocytic cells
Mechanisms of Chlamydia trachomatis entry into nonphagocytic cells
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DOI：
10.1128/iai.00106-07
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发表时间：
2007-08-01
影响因子：
3.1
通讯作者：
Stephens, Richard S.
中科院分区：
文献类型：
--
作者：
Hybiske, Kevin;Stephens, Richard S.
专性细胞内细菌沙眼衣原体的进入机制是通过各种进入模式所必需的蛋白质的功能破坏来检查的。RNA干扰用于破坏在网格蛋白介导的内吞作用（网格蛋白重链、动力蛋白-2、热休克70-kDa蛋白8、Arp2、接触蛋白和钙调蛋白）、小窝蛋白介导的内吞作用（caveolin-1、动力蛋白-2、Arp2、NSF和膜联蛋白II）、吞噬作用（RhoA、动力蛋白-2、Rac1和Arp2）和巨噬细胞作用（Pak1、Rac1和Arp2）中具有既定作用的蛋白。对转染小干扰rna的HeLa细胞进行比较定量PCR分析，以准确测定这些处理后沙眼衣原体的进入程度。与网格蛋白介导的内吞作用相关的关键结构和调节因子被发现参与衣原体的进入，而与小泡介导的内吞作用、吞噬作用和巨噬细胞作用无关。因此，沙眼衣原体的进入需要网格蛋白及其坐标辅助因子，尽管也利用了其他未表征的机制。
The mechanisms of entry for the obligate intracellular bacterium C. trachomatis were examined by functional disruption of proteins essential for various modes of entry. RNA interference was used to disrupt proteins with established roles in clathrin-mediated endocytosis (clathrin heavy chain, dynamin-2, heat shock 70-kDa protein 8, Arp2, cortactin, and calmodulin), caveola-mediated endocytosis (caveolin-1, dynamin-2, Arp2, NSF, and annexin II), phagocytosis (RhoA, dynamin-2, Rac1, and Arp2), and macropinocytosis (Pak1, Rac1, and Arp2). Comparative quantitative PCR analysis was performed on small interfering RNA-transfected HeLa cells to accurately determine the extent of C. trachomatis entry after these treatments. Key structural and regulatory factors associated with clathrin-mediated endocytosis were found to be involved in Chlamydia entry, whereas those for caveola-mediated endocytosis, phagocytosis, and macropinocytosis were not. Thus, clathrin and its coordinate accessory factors were required for entry of C. trachomatis, although additional, uncharacterized mechanisms are also utilized.