Weiss T W, Kvakan H, Kaun C, Prager M, Speidl W S, Zorn G, Pfaffenberger S, Huk I, Maurer G, Huber K, Wojta J
The Ludwig Boltzmann Foundation for Cardiovascular Research, Vienna, Austria.
J Clin Pathol. 2006 Nov;59(11):1186-90. doi: 10.1136/jcp.2005.034314. Epub 2006 Apr 27.
That infections with certain pathogens, by initiating an inflammatory response, may contribute to the development of atherosclerosis is suggested by clinical and experimental evidence.
To analyse atherosclerotic plaques of the carotid artery, samples of apparently healthy greater saphenous veins and circulating leucocytes from the same individual patients for the presence of Helicobacter pylori and Mycoplasma pneumoniae.
Samples from 36 patients undergoing carotid endarterectomy for symptomatic carotid artery stenosis were analysed by polymerase chain reaction for the presence of DNA specific for H. pylori and M. pneumoniae. IgG antibody titres against H. pylori and M pneumoniae and plasma levels of soluble E-selectin, soluble intercellular adhesion molecule-1 and soluble vascular cell adhesion molecule-1 were determined.
M. pneumoniae-specific DNA was detected in the atherosclerotic plaques of 13 of 36 (36.1%) patients, in the saphenous veins of 9 of 36 (25%) patients and in the leucocytes of 27 of 36 (75%) patients. No salient association was observed between the presence of M. pneumoniae-specific DNA in leucocytes and atherosclerotic plaques or veins. A marked correlation between the presence of M. pneumoniae in the respective specimens and the studied inflammatory markers or the presence of anti-M. pneumoniae antibodies was not observed. H. pylori-specific DNA could not be detected in the specimens tested.
The absence of H. pylori and the random distribution of M. pneumoniae in tissue samples obtained from patients with symptomatic carotid artery stenosis do not support a role for these pathogens in the development of atherosclerosis due to a direct interaction of the bacteria with the vasculature.
临床和实验证据表明，某些病原体感染通过引发炎症反应，可能促使动脉粥样硬化的发展。
分析同一患者的颈动脉粥样硬化斑块、外观健康的大隐静脉样本及循环白细胞，检测是否存在幽门螺杆菌和肺炎支原体。
对36例因有症状性颈动脉狭窄而接受颈动脉内膜切除术的患者样本，采用聚合酶链反应分析是否存在幽门螺杆菌和肺炎和肺炎支原体的特异性DNA。测定针对幽门螺杆菌和肺炎支原体的IgG抗体滴度，以及可溶性E选择素、可溶性细胞间黏附分子-1和可溶性血管细胞黏附分子-1的血浆水平。
在36例患者中的13例（36.1%）动脉粥样硬化斑块、9例（25%）大隐静脉及27例（75%）白细胞中检测到肺炎支原体特异性DNA。白细胞中肺炎支原体特异性DNA的存在与动脉粥样硬化斑块或静脉之间未观察到显著关联。在所检测的样本中，肺炎支原体的存在与所研究的炎症标志物或抗肺炎支原体抗体的存在之间未观察到明显相关性。在所检测的样本中未检测到幽门螺杆菌特异性DNA。
在有症状性颈动脉狭窄患者的组织样本中未检测到幽门螺杆菌，且肺炎支原体呈随机分布，这并不支持这些病原体通过与脉管系统直接相互作用在动脉粥样硬化发展中起作用。
