Generation of Chlamydia-induced atherosclerosis model mice

研究高血压转基因小鼠血管重构的发病机制和肺炎衣原体对小鼠的感染性，建立动脉粥样硬化疾病模型小鼠。1)携带人肾素和人血管紧张素原基因的高血压转基因小鼠，在胸主动脉血管平滑肌细胞去分化和细胞外基质积累的基础上，逐渐出现明显的血管肥大。以腹主动脉增生为主。将转基因高血压小鼠与C57BL/6对照小鼠分别饲喂致动脉粥样硬化饮食3个月，观察其主动脉粥样硬化病变情况。高血压转基因小鼠的动脉粥样硬化病变加速。2)通过抗体检测和PCR检测，证实了C57BL/6小鼠经鼻途径感染肺炎原体。感染小鼠在感染后3个月内无任何症状。在感染肺炎支原体的高血压转基因小鼠中发现动脉粥样硬化病变。

Pathgenesis of vascular remodeling in hypertensive transgenic mice and infectivity of Chlamydia pneumoniae to mice were examined to generate atherosclerotic disease model mice.1) The hypertensive transgenic mice carrying the human renin and human angiotensinogen gene progressively developed remarkable vascular hypertrophy composed of dedifferentiation of vascular smooth muscule cells and extracellular matrix accumulation in the thoracic aorta. The hyperplasia was predominant in the abdominal aorta. The hypertensive transgenic mice and C57BL/6 control mice fed with atherogenic diet for 3 months were compared in atherosclerotic lesion in aorta. Accelerated atherosclerotic lesion was demonstrated in the hypertensive transgenic mice.2) Infectivity of C. pneumoniae to mice from intranasal route was demonstrated in C57BL/6 mice by detection of antibody and PCR. Infected mice demonstrated no symptom during 3 months after infection. Atherosclerotic lesion was demonstrated in the hypertensive transgenic mice infected with C. pneumoniae.