Control mechanisms governing the infectivity of Chlamydia trachomatis for HeLa cells: the role of calmodulin.
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.
D000268:Adhesiveness; D002147:Calmodulin / Q000037:antagonists & inhibitors / Q000502:physiology*; D002692:Chlamydia trachomatis / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D006367:HeLa Cells / Q000187:drug effects / Q000382:microbiology* / Q000648:ultrastructure; D006801:Humans; D008854:Microscopy, Electron; D013912:Threonine / Q000378:metabolism; D014268:Trifluoperazine / Q000494:pharmacology
D002147:Calmodulin; D014268:Trifluoperazine; D013912:Threonine