In:
Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 100, No. 13 ( 1999-09-28), p. 1369-1373
Abstract:
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.
Type of Medium:
Online Resource
ISSN:
0009-7322
,
1524-4539
DOI:
10.1161/01.CIR.100.13.1369
Language:
English
Publisher:
Ovid Technologies (Wolters Kluwer Health)
Publication Date:
1999
detail.hit.zdb_id:
1466401-X
Bookmarklink