Muhlestein J B
Division of Cardiology, University of Utah, LDS Hospital, Salt Lake City, UT 84143, USA.
J Infect Dis. 2000 Jun;181 Suppl 3:S505-7. doi: 10.1086/315627.
In order to establish a causative relationship between Chlamydia pneumoniae and atherosclerosis, animal models have been proposed. In a rabbit model, arterial intimal thickening has been induced by direct intravascular and intranasal inoculation with C. pneumoniae. C. pneumoniae infection can induce significant acceleration of atherosclerosis in a mildly hyperlipidemic rabbit model but is prevented by treatment with azithromycin. Together these preliminary rabbit experiments suggest that C. pneumoniae may play a causative role in atherosclerosis. More animal studies are underway that are designed to address further mechanistic and therapeutic questions regarding the association between C. pneumoniae and atherosclerosis.
为了建立肺炎衣原体与动脉粥样硬化之间的因果关系，人们提出了动物模型。在一个兔模型中，通过直接血管内和鼻内接种肺炎衣原体诱导了动脉内膜增厚。肺炎衣原体感染可在轻度高脂血症兔模型中显著加速动脉粥样硬化，但阿奇霉素治疗可预防这种情况。这些初步的兔实验共同表明，肺炎衣原体可能在动脉粥样硬化中起因果作用。更多旨在解决有关肺炎衣原体与动脉粥样硬化之间关联的进一步机制和治疗问题的动物研究正在进行中。
