Campbell L A, Blessing E, Rosenfeld M, Lin T m, Kuo C
Department of Pathobiology, University of Washington, Seattle, WA 98195, USA.
J Infect Dis. 2000 Jun;181 Suppl 3:S508-13. doi: 10.1086/315629.
Mouse models were used to determine whether Chlamydia pneumoniae establishes chronic infection of the aorta and contributes to atherogenesis. Persistent infection of the aorta occurred in 11 of 31 hyperlipidemic apolipoprotein E-deficient (apoE(-/-)) mice but not in C57BL/6J mice fed a normal diet after a single inoculation and in both models following repeated inoculation with C. pneumoniae. Repeated inoculation of C57BL/6J mice resulted in inflammatory changes in the heart and aorta in 8 of 40 of mice; however, no atherosclerotic lesion development was observed. Repeated inoculation of apoE(-/-) mice resulted in a statistically significant increase in lesion area (n=43; P=.05). Although Chlamydia trachomatis disseminated to the aorta, persistent infection was not established and no statistically significant increase in lesion area occurred. These studies suggest that persistent infection of the aorta can lead to inflammatory changes in the absence of hyperlipidemia and accelerate lesion progress in concert with hyperlipidemia.
使用小鼠模型来确定肺炎衣原体是否会在主动脉中建立慢性感染并促进动脉粥样硬化的发生。在31只高脂血症载脂蛋白E缺陷（apoE(-/-)）小鼠中，有11只出现了主动脉的持续感染，但在单次接种后喂食正常饮食的C57BL/6J小鼠中未出现，且在两种模型中反复接种肺炎衣原体后也未出现。对C57BL/6J小鼠反复接种后，40只中有8只小鼠的心脏和主动脉出现了炎症变化；然而，未观察到动脉粥样硬化病变的发展。对apoE(-/-)小鼠反复接种导致病变面积有统计学意义的增加（n = 43；P = 0.05）。虽然沙眼衣原体扩散到了主动脉，但未建立持续感染，病变面积也未出现统计学意义的增加。这些研究表明，在没有高脂血症的情况下，主动脉的持续感染可导致炎症变化，并与高脂血症协同加速病变进展。
