Polymorphic membrane protein (PMP) 20 and PMP 21 of Chlamydia pneumoniae induce proinflammatory mediators in human endothelial cells in vitro by activation of the nuclear Factor-κB pathway
Polymorphic membrane protein (PMP) 20 and PMP 21 of Chlamydia pneumoniae induce proinflammatory mediators in human endothelial cells in vitro by activation of the nuclear Factor-κB pathway
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DOI：
10.1086/375827
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发表时间：
2003-07-01
影响因子：
6.4
通讯作者：
Wojta, J
中科院分区：
文献类型：
--
作者：
Niessner, A;Kaun, C;Wojta, J
我们测试了肺炎衣原体的多态性膜蛋白（PMPs）是否可能在触发人内皮细胞的炎症反应中发挥作用。在15种纯化的重组衣原体PMPs中，2种（PMP 20和PMP 21）在培养的人内皮细胞中剂量依赖性地增加炎症介质白细胞介素（IL）-6和MCP-1的产生; IL-8的产生也增加。当内皮细胞被活的C.在肺炎中，观察到IL-6、IL-8和MCP-1的产生增加。我们使用腺病毒诱导的IkappaBalpha-核因子（NF）-κ B抑制剂-的过表达来证明PMP 20和PMP 21通过激活NF-κ B途径增加人内皮细胞中IL-6和MCP-1的产生，因为在过表达IkappaBalpha的细胞中，用相应的PMP处理不会导致IL-6和MCP-1的产生增加。因此，C.肺炎链球菌可能通过其PMPs与内皮细胞的相互作用，参与动脉粥样硬化病变的发生和发展过程中的血管损伤过程。
We tested whether polymorphic membrane proteins (PMPs) of Chlamydia pneumoniae might play a role in triggering an inflammatory response in human endothelial cells. Of 15 purified, recombinant chlamydial PMPs tested, 2 (PMP 20 and PMP 21) dose-dependently increased the production of the inflammatory mediators interleukin (IL)-6 and monocyte chemoattractant protein-1 (MCP-1), in cultured human endothelial cells; production of IL-8 was also increased. When endothelial cells were infected by live C. pneumoniae, an increase in the production of IL-6, IL-8, and MCP-1 was seen. We used adenovirus-induced overexpression of IkappaBalpha-an inhibitor of nuclear factor (NF)-kappaB-to demonstrate that PMP 20 and PMP 21 increase the production of IL-6 and MCP-1 in human endothelial cells by activation of the NF-kappaB pathway, because, in cells overexpressing IkappaBalpha, treatment with the respective PMP did not result in increased production of IL-6 and MCP-1. Thus, C. pneumoniae could, by interactions of its PMPs with the endothelium, contribute to the process of vascular injury during the development and progression of atherosclerotic lesions.