Nuclear Factor–κB Activation in Endothelium byChlamydia pneumoniaewithout Active Infection | Zendy

Jefferson Baer | Zendy; Tracey V. du Laney | Zendy; Priscilla B. Wyrick | Zendy; Arlene S. McCain | Zendy; Thomas Fischer | Zendy; Elizabeth P. Merricks | Zendy; Albert S. Baldwin | Zendy; Timothy C. Nichols | Zendy

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Nuclear Factor–κB Activation in Endothelium byChlamydia pneumoniaewithout Active Infection

Author(s) -

Jefferson Baer,

Tracey V. du Laney,

Priscilla B. Wyrick,

Arlene S. McCain,

Thomas Fischer,

Elizabeth P. Merricks,

Albert S. Baldwin,

Timothy C. Nichols

Publication year - 2003

Publication title -

the journal of infectious diseases

Language(s) - Uncategorized

Resource type - Journals

SCImago Journal Rank - 2.69

H-Index - 252

eISSN - 1537-6613

pISSN - 0022-1899

DOI - 10.1086/378564

Subject(s) - chlamydia , chlamydophila pneumoniae , endothelium , repressor , biology , microbiology and biotechnology , transcription factor , chlamydiaceae , chlamydiales , endothelial activation , bacteria , immunology , virology , inflammation , gene , biochemistry , genetics

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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