Kälvegren Hanna, Majeed Meytham, Bengtsson Torbjörn
Division of Medical Microbiology, Department of Molecular and Clinical Medicine, Faculty of Health Sciences, Linköping University, Sweden.
Arterioscler Thromb Vasc Biol. 2003 Sep 1;23(9):1677-83. doi: 10.1161/01.ATV.0000084810.52464.D5. Epub 2003 Jul 3.
Evidence linking Chlamydia pneumoniae to atherosclerotic cardiovascular disease is expanding. Platelets are considered to play an essential role in cardiovascular diseases; however, so far platelets have not been associated with an infectious cause of atherosclerosis. This study aims to clarify the interaction between C pneumoniae and platelets and possibly present a novel mechanism in the pathogenesis of atherosclerosis.
The effects of C pneumoniae on platelet aggregation and secretion were assessed with lumiaggregometry, and the ability of C pneumoniae to bind to platelets and stimulate expression of P-selectin was analyzed with flow cytometry. We found that C pneumoniae, at a chlamydia:platelet ratio of 1:15, adheres to platelets and triggers P-selectin expression after 1 minute and causes an extensive aggregation and ATP secretion after 20 minutes of incubation. Inhibition of glycoprotein IIb/IIIa with Arg-Gly-Asp-Ser or abciximab markedly reduced C pneumoniae-induced platelet aggregation. Exposure of C pneumoniae to polymyxin B, but not elevated temperature, abolished the stimulatory effects on platelet activation, suggesting that chlamydial lipopolysaccharide has an active role. In contrast, other tested bacteria had no or only moderate effects on platelet functions.
Our findings demonstrate a new concept of how C pneumoniae activates platelets and thereby may cause atherosclerosis and thrombotic vascular occlusion.
将肺炎衣原体与动脉粥样硬化性心血管疾病联系起来的证据正在不断增加。血小板被认为在心血管疾病中起重要作用；然而，到目前为止，血小板尚未与动脉粥样硬化的感染性病因相关联。本研究旨在阐明肺炎衣原体与血小板之间的相互作用，并可能揭示动脉粥样硬化发病机制中的一种新机制。
采用光聚集法评估肺炎衣原体对血小板聚集和分泌的影响，并用流式细胞术分析肺炎衣原体与血小板结合及刺激P-选择素表达的能力。我们发现，肺炎衣原体以衣原体与血小板1:15的比例，在孵育1分钟后黏附于血小板并触发P-选择素表达，孵育20分钟后导致广泛的聚集和ATP分泌。用精氨酸-甘氨酸-天冬氨酸-丝氨酸（Arg-Gly-Asp-Ser）或阿昔单抗抑制糖蛋白IIb/IIIa可显著降低肺炎衣原体诱导的血小板聚集。将肺炎衣原体暴露于多黏菌素B而非升高温度后，其对血小板活化的刺激作用消失，这表明衣原体脂多糖起了积极作用。相比之下，其他受试细菌对血小板功能无影响或仅有中等影响。
我们的研究结果证明了肺炎衣原体激活血小板从而可能导致动脉粥样硬化和血栓性血管闭塞的新概念。
