Serologic and histopathologic study of Chlamydia pneumoniae infection in atherosclerosis: A possible pathogenetic mechanism of atherosclerosis induced Chlamydia pneumoniae

Chronic infection and inflammation have recently been implicated as importa nt etiologic agents for atherosclerosis in general and, in particular, isch emic heart disease. Several agents have been suggested as possible candidat es for the chronic inflammation including cytomegalovirus, Helicobacter pyl ori and Chlamydia pneumoniae. We hypothesized that a vascular infection wit h C. pneumoniae may induce a chronic inflammatory reaction in the host vasc ular tissue and activated inflammatory cells may express inflammatory media tors such as cyclooxygenase-2 (COX-2) and matrix metalloproteinases (MMPs). At first, we evaluated the relationship between C. pneumoniae infection an d atherosclerosis indirectly by serologic study, and then, to confirm our h ypothesis, we performed an immunohistochemical study of atherosclerotic pla ques. The seropositive rate of anti-Chlamydia pneumoniae IgG was higher in the disease group (Group I, 59.8%, n = 254) than in the negative control gr oup (Group III, 47.4%, n = 97) (p = 0.041), but the anci-Chlamydia pneumoni ae IgA was not different in seropositivity between the two groups (Group I, 64.6%; Group III, 57.7%). The simultaneous seropositive rates of both IgG and IgA were 56.7% in Group I and 43.3% in Group III (p = 0.033). Tn subgro ups without the conventional risk factors of atherosclerosis, these finding s were more prominent. Furthermore, we performed immunohistochemical staini ng on the atherosclerotic aortic tissues obtained from patients that were s eropositive to C. pneumoniae (n = 5), by using antibodies to C. pneumoniae, COX-2, and MMP-9. The immunoreactivity for COX-2 and MMP-9 increased in th e atherosclerotic plaques itself, predominantly in the surrounding area of immunoreactive C. pneumoniae. These findings support our hypothesis and C. pneumoniae may participate in a pathogenetic mechanism for atherogenesis or progression of atherosclerosis. The present study may open a promising per spective concerning future therapeutic trials of chronic inflammation relat ed atherogenesis under pathophysiological conditions.