CHLAMYDIA SPECIES INFECT HUMAN VASCULAR ENDOTHELIAL-CELLS AND INDUCE PROCOAGULANT ACTIVITY

Background: Chlamydia pneumoniae infections have been linked with myoc ardial infarction, stroke, and the development of atherosclerosis by e pidemiologic studies, immunohistochemical studies, and electron micros copic studies, The mechanisms underlying this association are unknown. Methods: Using cultured human venous endothelial cells, we investigat ed whether C pneumoniae, C trachomatis (types H and L2/434/BU) could i nfect these cells, The ability of infected cells to express procoagula nt (tissue factor) activity was also measured using clotting and chrom ogenic substrate assays, Adhesion of platelets to chlamydia-infected c ells was also quantitated. Results: We found that C pneumoniae, C trac homatis type H, and C trachomatis L2/434/BU could infect cultured huma n umbilical vein endothelial cells and stimulate a 4-fold increase in expression of tissue factor, which reached a peak 18 hours postinfecti on, Tissue factor expression was enhanced even in the presence of tetr acycline, suggesting that the chlamydial factor responsible for stimul ating synthesis of endothelial cell tissue factor was preformed. Plate let adhesion was significantly enhanced when endothelial cells were in fected by chlamydia species, Conclusions: These in vitro studies sugge st possible pathogenic mechanisms that may explain the association of thrombotic events with C pneumoniae infection, including pathologicall y enhanced production of tissue factor by human endothelial cells and enhanced focal platelet deposition.