Chlamydia pneumoniae infection of vascular smooth muscle and endothelial cells activates NF-κB and induces tissue factor and PAI-1 expression : A potential link to accelerated arteriosclerosis

• Published in: Circulation (New York, N.Y.) N.Y.), 1999-09, Vol.100 (13), p.1369-1373
• Main Authors: DECHEND, R, MAASS, M, GIEFFERS, J, DIETZ, R, SCHEIDEREIT, C, LEUTZ, A, GULBA, D. C
• Format: Article
• Language: English
• Subjects: Atherosclerosis (general aspects, experimental research); Biological and medical sciences; Blood and lymphatic vessels; Cardiology. Vascular system; Medical sciences
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/01.CIR.100.13.1369

Background —Recent reports link C. pneumoniae infection of arteriosclerotic lesions to the precipitation of acute coronary syndromes, which also feature tissue factor and plasminogen activator inhibitor 1 (PAI-1) overexpression. We investigated whether or not C. pneumoniae can induce thrombogenicity by upregulation of procoagulant proteins. Methods and Results —Human vascular endothelial and smooth muscle cells were infected with a strain of C. pneumoniae isolated from an arteriosclerotic coronary artery. Tissue factor, PAI-1, and interleukin-6 expression was increased in infected cells. Concomitantly, NF-κB was activated and IκBα degraded. p50/p65 heterodimers were identified as the components responsible for the NF-κB activity. Conclusions —These data provide evidence that C. pneumoniae infection can induce procoagulant protein and proinflammatory cytokine expression. This cellular response is accompanied by activation of NF-κB. Our results demonstrate how C. pneumoniae infection may initiate acute coronary syndromes.