Nuclear Factor–κB Activation in Endothelium by Chlamydia pneumoniae without Active Infection

Causative molecular mechanisms accounting for the potential link between Chlamydia pneumoniae and atherosclerosis are unknown. Formalin and heat-inactivated C. pneumoniae activated the transcription factor nuclear factor (NF)-KB in cultured porcine endothelium and up-regulated the expression of E-selectin messenger RNA and protein. This up-regulation was abolished by an IKB super-repressor, an NF-KB-specific inhibitor. Live bacteria are not necessary for the activation of endothelial NF-KB, and C. pneumoniae may contribute to atherogenesis without active infection.