Research article

Chlamydia pneumoniae aggravates vein graft intimal hyperplasia in a rat model

Geoffrey TL Kloppenburg¹ , Rick de Graaf² , Gert ELM Grauls¹ , Cathrien A Bruggeman¹ and Frank R Stassen¹

¹  Cardiovascular Research Institute Maastricht, Department of Medical Microbiology, Academic Hospital Maastricht/Maastricht University, Maastricht, MD Maastricht, The Netherlands

²  Cardiovascular Research Institute Maastricht, Department of Radiology, Academic Hospital Maastricht/Maastricht University, Maastricht, P.O. Box 616 6200 MD Maastricht, The Netherlands

author email corresponding author email

BMC Microbiology 2007, 7:111doi:10.1186/1471-2180-7-111

Published:	6 December 2007

Abstract

Background

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.

Results

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/μm² 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.

Conclusion

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.