Journal
CARDIOVASCULAR RESEARCH
Volume 57, Issue 3, Pages 834-842Publisher
OXFORD UNIV PRESS
DOI: 10.1016/S0008-6363(02)00787-3
Keywords
atherosclerosis; coronary disease; infection/inflammation; macrophages
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Objectives: We evaluated the role of intracoronary. intrapulmonary and macrophage-mediated delivery of C. pneumoniae (Cp) oil coronary lesion formation. Methods: Pigs were allocated to one of three coronary protocols (intracoronary. macrophage or control groups) or to a fourth-a pulmonary group. fit the intracoronary group Cp was injected into the wall of the left anterior descending (LAD) and right coronary arteries (RCA) and vehicle into the circumflex (CX). In the macrophage group autologous macrophages preincubated with Cp or not were injected into the LAD and CX wall, respectively. Animals in the control group received vehicle in LAD and CX. In the pulmonary group aerosolised Cp was given intrabronchially. after a single injection of vehicle into the LAD wall. Delivery into the coronary artery wall was performed with a balloon catheter with low-profile injector ports. Results: Seroconversion occurred in the following proportions: 5/6 (intracoronar group). 4/5 (macrophage group), 0/6 (control group). and 1/6 (intrapulmonary group). Significantly higher maximal intimal thickness (MIT) was observed in LADs of intracoronary and pulmonary groups when compared to corresponding CXs. The presence of Cp antigen was associated with higher MIT (r=0.73 P<0.0001). Injection of macrophages into the coronary artery wall did not induce proliferation. Arteries without coronary interventions were morphologically normal. Conclusions: Intracoronary and intrapulmonary but not macrophage-mediated Cp inoculation were associated with moderate intimal proliferation in the absence of a lipid-rich diet. Pre-existing coronary lesions seem a prerequisite for Cp-induced proliferation. (C) 2003 European Society of Cardiology. Published by Elsevier Science B.V. All rights reserved.
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