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肺炎衣原体与心血管疾病

Chlamydia pneumoniae and Cardiovascular Disease.

作者信息

Kolia Maria, Fong Ignatius William

机构信息

Division of Infectious Disease, St. Michael's Hospital, 30 Bond Street, Room 4179V, Toronto, Ontario, M5W 1W8, Canada.

出版信息

Curr Infect Dis Rep. 2002 Feb;4(1):35-43. doi: 10.1007/s11908-002-0065-4.

Abstract

Chlamydia pneumoniae, a respiratory pathogen, has been suggested as a risk factor for cardiovascular disease. Epidemiologic data are very controversial. Histopathologic and microbiologic studies have established an association between atherosclerosis and presence of C. pneumoniae, consistently finding C. pneumoniae DNA and antigens in atherosclerotic arteries. C. pneumoniae has been cultured from atherosclerotic arteries in several centers. An etiologic role for C. pneumoniae in initiation, acceleration of atherosclerosis, and/or acute ischemia remains debatable. In vitro studies have shown that C. pneumoniae can induce foam cell formation, low-density lipoprotein oxidation, and proinflammatory and procoagulant cytokine expression. Animal models of de novo initiation or enhancement of atherosclerosis have been developed. Preliminary trials of secondary prevention of coronary artery disease complications by antimicrobial agents show modest results. Better diagnostic tools, more diverse animal models, and clinical trials of primary prevention are needed. Meanwhile, results of ongoing large clinical trials on secondary prevention are eagerly awaited, but may not be definitive.

摘要

肺炎衣原体是一种呼吸道病原体,已被认为是心血管疾病的一个危险因素。流行病学数据极具争议性。组织病理学和微生物学研究已证实动脉粥样硬化与肺炎衣原体的存在之间存在关联,在动脉粥样硬化动脉中持续发现肺炎衣原体DNA和抗原。多个中心已从动脉粥样硬化动脉中培养出肺炎衣原体。肺炎衣原体在动脉粥样硬化的起始、加速和/或急性缺血中所起的病因学作用仍存在争议。体外研究表明,肺炎衣原体可诱导泡沫细胞形成、低密度脂蛋白氧化以及促炎和促凝血细胞因子表达。已建立了动脉粥样硬化从头起始或加重的动物模型。抗菌药物对冠状动脉疾病并发症二级预防的初步试验结果一般。需要更好的诊断工具、更多样化的动物模型以及一级预防的临床试验。与此同时,人们急切期待正在进行的二级预防大型临床试验的结果,但结果可能并不确定。

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