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首页> 外文期刊>Clinical microbiology and infection: European Society of Clinical Microbiology and Infectious Diseases >Chlamydia pneumoniae and atherosclerosis -- what we know and what we don't.
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Chlamydia pneumoniae and atherosclerosis -- what we know and what we don't.

机译:肺炎衣原体和动脉粥样硬化-我们所知道的和我们所不知道的。

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摘要

The clinical manifestations of atherosclerosis include coronary artery disease (CAD), stroke, abdominal aortic aneurysm and peripheral vascular disease. World-wide, CAD and stroke are the leading causes of death and disability. The recognition of atherosclerosis as an inflammatory disease in its genesis, progression and ultimate clinical manifestations has created an interesting area of vascular research. Apart from those well-known traditional risk factors for atherosclerosis, novel and potentially treatable atherosclerotic risk factors such as homocysteine (an amino acid derived from the metabolism of dietary methionine that induces vascular endothelial dysfunction) and infections have emerged. In fact, the century-old 'infectious' hypothesis of atherosclerosis has implicated a number of micro-organisms that may act as contributing inflammatory stimuli. Although cytomegalovirus, Helicobacter pylori and Chlamydia pneumoniae are the three micro-organisms most extensively studied, this review will focus on C. pneumoniae. Collaborative efforts from many disciplines have resulted in the accumulation of evidence from seroepidemiological, pathological, animal model, immunological and antibiotic intervention studies, linking C. pneumoniae with atherosclerosis. Seroepidemiological observations provide circumstantial evidence, which is weak in most prospective studies. Pathological studies have demonstrated the preferential existence of C. pneumoniae in atherosclerotic plaque tissues, while animal model experiments have shown the induction of atherosclerosis by C. pneumoniae. Finally, immunological processes whereby C. pneumoniae could participate in key atherogenic and atherothrombotic events have also been identified. Although benefits of the secondary prevention of atherosclerosis have been demonstrated in some antibiotic intervention studies, a number of negative studies have also emerged. The results of the ongoing large prospective human antibiotic intervention trials may help to finally establish if there is a causal link between C. pneumoniae infection and atherosclerosis.
机译:动脉粥样硬化的临床表现包括冠状动脉疾病(CAD),中风,腹主动脉瘤和周围血管疾病。在全球范围内,CAD和中风是导致死亡和残疾的主要原因。在其发生,发展和最终的临床表现中将动脉粥样硬化识别为炎性疾病,这已成为血管研究的一个有趣领域。除了那些众所周知的传统的动脉粥样硬化危险因素外,还出现了新的且可能可治疗的动脉粥样硬化危险因素,例如高半胱氨酸(一种高蛋白饮食氨基酸的新陈代谢引起的氨基酸,可引起血管内皮功能障碍)和感染。实际上,具有百年历史的动脉粥样硬化“感染性”假说已经牵涉到许多微生物,它们可能是促发炎性刺激的因素。尽管巨细胞病毒,幽门螺杆菌和肺炎衣原体是研究最广泛的三种微生物,但本文将重点讨论肺炎衣原体。许多学科的共同努力导致了血清流行病学,病理学,动物模型,免疫学和抗生素干预研究的证据积累,将肺炎衣原体与动脉粥样硬化联系起来。血清流行病学观察提供了间接证据,在大多数前瞻性研究中这是薄弱的。病理研究表明,动脉粥样硬化斑块组织中优先存在肺炎衣原体,而动物模型实验表明,肺炎衣原体可诱发肺动脉粥样硬化。最后,还确定了肺炎衣原体可以参与关键的动脉粥样硬化和动脉粥样硬化形成事件的免疫学过程。尽管在某些抗生素干预研究中已证明了二级预防动脉粥样硬化的益处,但也出现了许多阴性研究。正在进行的大规模前瞻性人类抗生素干预试验的结果可能有助于最终确定肺炎衣原体感染与动脉粥样硬化之间是否存在因果关系。

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