ALLOGRAFT MODELS Chlamydia Pneumoniae Infection Is Not Associated With Chronic Transplant Dysfunction in a Rat Aortic Allograft Model G.T.L. Kloppenburg, H.C. Graeler, G.E.L.M. Grauls, C.A. Bruggeman, and F.R. Stassen ABSTRACT Long-term survival of solid-organ transplants is limited as a result of chronic transplant dysfunction (CTD), which is characterized by occlusion of intragraft vascular tissue due to myointimal hyperplasia. Recent studies have shown a role for infections in vascular pathologies. For example, Chlamydia pneumoniae (Cpn) has been shown to aggravate atherosclerosis, and Cpn immunoglobulin (Ig)G titers correlate with severity of allograft atherosclerosis after cardiac transplantation. In this study, we evaluated the effect of Cpn infection on CTD using a rat aortic allograft model. Orthotopic abdominal aorta transplantations (Tx) were performed with Brown Norway rats as donors and Lewis rats as recipients. Rats were humanely killed at 1 or 8 weeks after surgery. The graft was processed for DNA isolation and histological examination. Influx of macrophages and T cells was assessed using immunohistochemistry. At 1 week after Tx, the perivascular influx of inflammatory cells in the graft was not affected by Cpn infection. Furthermore, only limited numbers of Cpn DNA copies were found in the graft at 1 week after Tx. In addition, Cpn did not alter the severity of myointimal hyperplasia in the rat aortic allograft model at 8 weeks after surgery. Our data suggested that, in the rat aortic allograft model, Cpn infection did not influence the influx of inflammatory cells or the severity of CTD. O RGAN transplantation has become an increasingly successful medical treatment for patients with end- stage organ failure. However, despite improvements in immunosuppressive drug therapy and treatment of acute rejection, long-term survival of solid-organ transplants is limited as a result of chronic transplant dysfunction (CTD). In the majority of organs, CTD is characterized by a persistent perivascular inflammation, which results in a diffuse multifocal myointimal hyperplasia and inadequate vascular remodeling resulting in intimal narrowing of all the vessels in the graft. 1 Major risk factors for CTD are humoral and cellular immune responses, hyperlipidemia, and viral infections. Regarding the latter, cytomegalovirus (CMV) in particular has been associated with CTD. Multi- From the Department of Medical Microbiology and Maastricht Infection Centre, University Hospital Maastricht, Maastricht, the Netherlands. Address reprint requests to F.R. Stassen, Department of Medical Microbiology and Maastricht Infection Centre, University Hospital Maastricht, P. Debyelaan 25, P.O. 5800, 6202 AZ Maastricht, the Netherlands. E-mail: f.stassen@medmic.unimaas.nl © 2007 by Elsevier Inc. All rights reserved. 0041-1345/07/$–see front matter 360 Park Avenue South, New York, NY 10010-1710 doi:10.1016/j.transproceed.2006.10.012 Transplantation Proceedings, 39, 261–267 (2007) 261