Nuclear factor-kappaB activation in endothelium by Chlamydia pneumoniae without active infection.

Baer, Jefferson T; Du Laney, Tracey V; Wyrick, Priscilla B; McCain, Arlene S; Fischer, Thomas A; Merricks, Elizabeth P; Baldwin, Albert S; Nichols, Timothy C · J Infect Dis · 2003

basic_science · Level V

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Abstract

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

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