Chlamydia pneumoniae infection of vascular smooth muscle and endothelial cells activates NF-κB and induces tissue factor and PAI-1 expression -: A potential link to accelerated arteriosclerosis

Background-Recent reports link C. pneumoniae infection of arteriosclerotic lesions to the precipitation of acute coronary syndromes, which also feature tissue factor and plasminogen activator inhibitor 1 (PAI-1) overexpression. We investigated whether or not C. pneumoniae can induce thrombogenicity by upregulation of procoagulant proteins. Methods and Results-Human vascular endothelial and smooth muscle cells were infected with a strain of C. pneumoniae isolated from an arteriosclerotic coronary artery. Tissue factor, PAI-1: and interleukin-6 expression was increased in infected cells. Concomitantly, NF-kappa B was activated and I kappa B alpha degraded. p50/p65 heterodimers were identified as the components responsible for the NF-kappa B activity. Conclusions-These data provide evidence that C. pneumoniae infection can induce procoagulant protein and proinflammatory cytokine expression. This cellular response is accompanied by activation of NF-kappa B. Our results demonstrate how C. pneumoniae infection may initiate acute coronary syndromes.