Rapid, Transient Phosphatidylserine Externalization Induced in Host Cells by Infection withChlamydiaspp

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Abstract
Chlamydiaorganisms are obligate intracellular bacterial pathogens responsible for a range of human diseases. Persistent infection or reinfection withChlamydia trachomatisleads to scarring of ocular or genital tissues, andChlamydia pneumoniaeinfection is associated with the development of atherosclerosis. We demonstrate thatC. trachomatisandC. pneumoniaeinfection in vitro elicits the externalization of the lipid phosphatidylserine on the surface of human epithelial, endothelial, granulocytic, and monocytic cells. Phosphatidylserine externalization is associated with cellular development, differentiation, and death. Infection-induced phosphatidylserine externalization was immediate, transient, calcium dependent, and infectious dose dependent and was unaffected by a broad-spectrum caspase inhibitor.Chlamydia-infected cells accelerated plasma clotting and increased the macrophage phagocytosis of infected cells that was phosphatidylserine dependent. The rapid externalization of phosphatidylserine by infected cells may be an important factor in the pathogenesis of chlamydial infections.