Serologic and histopathologic study of Chlamydia pneumoniae infection in atherosclerosis: a possible pathogenetic mechanism of atherosclerosis induced by Chlamydia pneumoniae.
10.3349/ymj.2000.41.3.319
- Author:
Young Goo SONG
1
;
Hyuck Moon KWON
;
June Myung KIM
;
Bum Kee HONG
;
Dong Soo KIM
;
Ae Jung HUH
;
Kyung Hee CHANG
;
Hyo Yul KIM
;
Tae Soo KANG
;
Byung Kwon LEE
;
Dong Hoon CHOI
;
Yang Soo JANG
;
Hyun Seung KIM
Author Information
1. Department of Internal Medicine, Cardiovascular Research Institute, Yonsei University College of Medicine, Seoul, Korea. kwonhm @yumc.yonsei.ac.kr
- Publication Type:Original Article
- Keywords:
Chlamydia pneumoniae;
atherosclerosis;
cyclooxygenase-2 (COX-2);
matrix metalloproteinases (MMPs)
- MeSH:
Aged;
Arteriosclerosis/pathology*;
Arteriosclerosis/microbiology*;
Arteriosclerosis/metabolism;
Chlamydia Infections/complications*;
Chlamydophila pneumoniae;
Female;
Gelatinase B/metabolism;
Human;
Isoenzymes/metabolism;
Male;
Middle Age;
Prostaglandin-Endoperoxide Synthase/metabolism;
Serologic Tests*
- From:Yonsei Medical Journal
2000;41(3):319-327
- CountryRepublic of Korea
- Language:English
-
Abstract:
Chronic infection and inflammation have recently been implicated as important etiologic agents for atherosclerosis in general and, in particular, ischemic heart disease. Several agents have been suggested as possible candidates for the chronic inflammation including cytomegalovirus, Helicobacter pylori and Chlamydia pneumoniae. We hypothesized that a vascular infection with C. pneumoniae may induce a chronic inflammatory reaction in the host vascular tissue and activated inflammatory cells may express inflammatory mediators such as cyclooxygenase-2 (COX-2) and matrix metalloproteinases (MMPs). At first, we evaluated the relationship between C. pneumoniae infection and atherosclerosis indirectly by serologic study, and then, to confirm our hypothesis, we performed an immunohistochemical study of atherosclerotic plaques. 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 group (Group III, 47.4%, n = 97) (p = 0.041), but the anti-Chlamydia pneumoniae 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). In subgroups without the conventional risk factors of atherosclerosis, these findings were more prominent. Furthermore, we performed immunohistochemical staining on the atherosclerotic aortic tissues obtained from patients that were seropositive 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 the 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 perspective concerning future therapeutic trials of chronic inflammation related atherogenesis under pathophysiological conditions.
