Chlamydia pneumoniae infection of endothelial cells induces transcriptional activation of platelet-derived growth factor-B: a potential link to intimal thickening in a rabbit model of atherosclerosis

Smooth muscle cell (SMC) proliferation and intimal thickening are hallmark features of ath-erosclerotic disease, and Chlamydia pneumoniae may contribute to atherogenesis by imparting biological effects on SMCs. An in vitro endothelial cell model and a normocholesterolemic rabbit model were used to test the hypothesis that infection with C. pneumoniae induces SMC growth factor production, SMC proliferation, and aortic intimal thickening. Using reverse-transcriptase polymerase chain reaction, it was demonstrated that C. pneumoniae infection of endothelial cells induced platelet-derived growth factor (PDGF) – B messenger RNA expression. In C. pneumo-niae – infected rabbits, maximum intimal thickness (MIT) was significantly greater than that in uninfected animals (P,.0001). MIT correlated with the presence of C. pneumoniae antigen (P .043) and PDGF-B (P .002) in aortic tissues, and C. pneumoniae antigen was indepen-dently correlated with the presence of PDGF-B in aortic tissues (P .009). These results suggest that C. pneumoniae – induced SMC proliferation and intimal thickening may be mediated through PDGF-B and may be a molecular mechanism by which C. pneumoniae infection could contribute to atherogenesis. Chlamydia pneumoniae is an obligate intracellular pathoge