Nuclear factor-kappaB 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)-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.
Baer
Jefferson T
JT
Department of Pathology, University of North Carolina School of Medicine, North Carolina 27516, USA.
Du Laney
Tracey V
TV
Wyrick
Priscilla B
PB
McCain
Arlene S
AS
Fischer
Thomas A
TA
Merricks
Elizabeth P
EP
Baldwin
Albert S
AS
Nichols
Timothy C
TC
D000818:Animals; D001011:Aorta / Q000382:microbiology; D002478:Cells, Cultured; D016993:Chlamydophila pneumoniae / Q000187:drug effects / Q000254:growth & development / Q000472:pathogenicity*; D019040:E-Selectin / Q000378:metabolism; D004730:Endothelium, Vascular / Q000166:cytology / Q000382:microbiology*; D005557:Formaldehyde / Q000494:pharmacology; D006358:Hot Temperature; D006801:Humans; D016328:NF-kappa B / Q000378:metabolism*; D013552:Swine; D015533:Transcriptional Activation; D015854:Up-Regulation
D019040:E-Selectin; D016328:NF-kappa B; D005557:Formaldehyde