Serologic and histopathologic study of Chlamydia pneumoniae infection in atherosclerosis

a possible pathogenetic mechanism of atherosclerosis induced by Chlamydia pneumoniae.

Y. G. Song, H. M. Kwon, J. M. Kim, B. K. Hong, D. S. Kim, A. J. Huh, K. H. Chang, H. Y. Kim, T. S. Kang, B. K. Lee, Donghoon Choi, Yangsoo Jang, H. S. Kim

Research output: Contribution to journalArticle

18 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)319-327
Number of pages9
JournalYonsei Medical Journal
Volume41
Issue number3
DOIs
Publication statusPublished - 2000 Jan 1

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Chlamydophila pneumoniae
Chlamydia Infections
Atherosclerosis
Cyclooxygenase 2
Matrix Metalloproteinase 9
Atherosclerotic Plaques
Inflammation
Immunoglobulin A
Blood Vessels
Immunoglobulin G
Infection
Matrix Metalloproteinases
Cytomegalovirus
Helicobacter pylori
Myocardial Ischemia
Staining and Labeling
Control Groups
Antibodies

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

Song, Y. G. ; Kwon, H. M. ; Kim, J. M. ; Hong, B. K. ; Kim, D. S. ; Huh, A. J. ; Chang, K. H. ; Kim, H. Y. ; Kang, T. S. ; Lee, B. K. ; Choi, Donghoon ; Jang, Yangsoo ; Kim, H. S. / Serologic and histopathologic study of Chlamydia pneumoniae infection in atherosclerosis : a possible pathogenetic mechanism of atherosclerosis induced by Chlamydia pneumoniae. In: Yonsei Medical Journal. 2000 ; Vol. 41, No. 3. pp. 319-327.
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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.",
author = "Song, {Y. G.} and Kwon, {H. M.} and Kim, {J. M.} and Hong, {B. K.} and Kim, {D. S.} and Huh, {A. J.} and Chang, {K. H.} and Kim, {H. Y.} and Kang, {T. S.} and Lee, {B. K.} and Donghoon Choi and Yangsoo Jang and Kim, {H. S.}",
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Serologic and histopathologic study of Chlamydia pneumoniae infection in atherosclerosis : a possible pathogenetic mechanism of atherosclerosis induced by Chlamydia pneumoniae. / Song, Y. G.; Kwon, H. M.; Kim, J. M.; Hong, B. K.; Kim, D. S.; Huh, A. J.; Chang, K. H.; Kim, H. Y.; Kang, T. S.; Lee, B. K.; Choi, Donghoon; Jang, Yangsoo; Kim, H. S.

In: Yonsei Medical Journal, Vol. 41, No. 3, 01.01.2000, p. 319-327.

Research output: Contribution to journalArticle

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T1 - Serologic and histopathologic study of Chlamydia pneumoniae infection in atherosclerosis

T2 - a possible pathogenetic mechanism of atherosclerosis induced by Chlamydia pneumoniae.

AU - Song, Y. G.

AU - Kwon, H. M.

AU - Kim, J. M.

AU - Hong, B. K.

AU - Kim, D. S.

AU - Huh, A. J.

AU - Chang, K. H.

AU - Kim, H. Y.

AU - Kang, T. S.

AU - Lee, B. K.

AU - Choi, Donghoon

AU - Jang, Yangsoo

AU - Kim, H. S.

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Y1 - 2000/1/1

N2 - 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.

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