Murray A, Ward M E
J Gen Microbiol. 1984 Jan;130(1):193-201. doi: 10.1099/00221287-130-1-193.
Adhesion of the obligate intracellular bacterium Chlamydia trachomatis to host cells is associated with a flux of Ca2+ across the cell membrane, and infection is enhanced by treatment of host cells with Ca2+ ionophore. The possibility that Ca2+ might interact with host cell Ca2+ regulatory proteins to promote chlamydial infection was investigated. Treatment of HeLa 229 cells with the calmodulin inhibitors pimozide, trifluoperazine, chlorpromazine, promethazine or haloperidol reduced chlamydial infectivity as measured by inclusion counting or the specific incorporation of [3H]threonine. The inhibitory effect was reversible, dose-related and shown to be associated with impairment of chlamydial adhesion and uptake by the host cells. This effect was clearly distinguished from the delayed maturation of chlamydiae due to continuous exposure to calmodulin inhibitors which may result from a decrease in the availability of high energy compounds from the host cells necessary for chlamydial growth. The possible mechanisms for calmodulin-mediated chlamydial endocytosis are discussed.
专性胞内细菌沙眼衣原体与宿主细胞的黏附与Ca2+跨细胞膜流动有关，用Ca2+离子载体处理宿主细胞可增强感染。研究了Ca2+可能与宿主细胞Ca2+调节蛋白相互作用以促进衣原体感染的可能性。用钙调蛋白抑制剂匹莫齐特、三氟拉嗪、氯丙嗪、异丙嗪或氟哌啶醇处理HeLa 229细胞，通过包涵体计数或[3H]苏氨酸的特异性掺入来测量，可降低衣原体感染性。抑制作用是可逆的、剂量相关的，并且表明与宿主细胞对衣原体的黏附和摄取受损有关。这种作用与由于持续暴露于钙调蛋白抑制剂导致的衣原体延迟成熟明显不同，后者可能是由于衣原体生长所需的宿主细胞高能化合物可用性降低所致。讨论了钙调蛋白介导衣原体胞吞作用的可能机制。
