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)–κB in cultured porcine endothelium and up-regulated the expression of E-selectin messenger RNA and protein. This up-regulation was abolished by an IκB super-repressor, an NF-κB–specific inhibitor. Live bacteria are not necessary for the activation of endothelial NF-κB, and C. pneumoniae may contribute to atherogenesis without active infection