Kloppenburg Geoffrey T L, de Graaf Rick, Grauls Gert E L M, Bruggeman Cathrien A, Stassen Frank R
Cardiovascular Research Institute Maastricht, Department of Medical Microbiology, Academic Hospital Maastricht/Maastricht University, Maastricht, MD Maastricht, The Netherlands.
BMC Microbiol. 2007 Dec 6;7:111. doi: 10.1186/1471-2180-7-111.
Along with angioplasty, autologus vein grafts are commonly used for artery bypass grafting in patients with advanced arterial stenosis and drug-resistant angina pectoris. Although initially a successful procedure, long-term functionality is limited due to proliferation and migration of smooth muscle cells. Like in atherosclerosis, common chronic infections caused by viruses and bacteria may contribute to this process of vein graft failure. Here we investigated the possible role of Chlamydia pneumoniae (Cpn) in the pathogenesis of venous graft failure in an experimental animal model. In 2 groups (n = 10 rats/group), an epigastric vein-to-common femoral artery interposition graft was placed. Immediately thereafter, rats were infected with Cpn (5*108 IFU) or injected with control solutions. Rats were sacrificed three weeks after surgery and the grafts were harvested for morphometrical and immunohistochemical analysis.
Cpn administration immediately after vein grafting resulted in a significant increase in medial cross-sectional area, wall thickness and total wall area. There were no significant differences in T-cell or macrophage influx. Likewise, although positive immunostaining for both HSP60 and CRP could be detected, no differences were found between groups. Based on the observation that the number of cells/microm2 was also not altered, we conclude that Cpn infection stimulates smooth muscle cell proliferation by hereunto unknown molecular mechanisms, resulting in a significant increase in intimal hyperplasia.
In conclusion, in a well defined animal model we present here for the first time evidence for a role of Chlamydia pneumoniae in the process of venous graft failure.
除血管成形术外，自体静脉移植物常用于患有晚期动脉狭窄和耐药性心绞痛患者的动脉搭桥手术。尽管该手术最初很成功，但由于平滑肌细胞的增殖和迁移，其长期功能受到限制。与动脉粥样硬化一样，由病毒和细菌引起的常见慢性感染可能导致静脉移植物失败的这一过程。在此，我们在实验动物模型中研究了肺炎衣原体（Cpn）在静脉移植物失败发病机制中的可能作用。将两组（每组n = 10只大鼠）进行腹壁静脉至股总动脉的间置移植。此后立即给大鼠感染Cpn（5×108 IFU）或注射对照溶液。术后三周处死大鼠，取出移植物进行形态计量学和免疫组织化学分析。
静脉移植后立即给予Cpn导致中膜横截面积、壁厚和总壁面积显著增加。T细胞或巨噬细胞浸润无显著差异。同样，尽管可检测到HSP60和CRP的阳性免疫染色，但两组之间未发现差异。基于细胞数/平方微米也未改变的观察结果，我们得出结论，Cpn感染通过迄今未知的分子机制刺激平滑肌细胞增殖，导致内膜增生显著增加。
总之，在一个明确的动物模型中，我们首次在此提供了肺炎衣原体在静脉移植物失败过程中起作用的证据。
