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
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
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DOI：
10.1161/01.cir.100.13.1369
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发表时间：
1999-09-28
期刊：
影响因子：
37.8
通讯作者：
Gulba, DC
中科院分区：
文献类型：
--
作者：
Dechend, R;Maass, M;Gulba, DC
最近的报道将肺炎c感染动脉硬化病变与急性冠状动脉综合征的沉淀联系起来，急性冠状动脉综合征也具有组织因子和纤溶酶原激活物抑制剂1 （PAI-1）过表达的特征。我们研究了肺炎梭菌是否可以通过上调促凝蛋白诱导血栓形成。方法与结果：用从冠状动脉硬化区分离的肺炎衣原体感染人血管内皮细胞和平滑肌细胞。感染细胞中组织因子、PAI-1、白细胞介素-6表达升高。同时，nf - κ B被激活，I κ B α被降解。p50/p65异源二聚体被确定为NF-kappa B活性的组成部分。结论：肺炎梭菌感染可诱导促凝蛋白和促炎细胞因子的表达。这种细胞反应伴随着NF-kappa b的激活。我们的研究结果证明了肺炎梭菌感染如何引发急性冠状动脉综合征。
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-kappa B was activated and I kappa B alpha degraded. p50/p65 heterodimers were identified as the components responsible for the NF-kappa B 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-kappa B. Our results demonstrate how C. pneumoniae infection may initiate acute coronary syndromes.