© 2000 American Heart Association, Inc.
Atherosclerosis and Lipoproteins |
Detection of Chlamydia pneumoniae–Reactive T Lymphocytes in Human Atherosclerotic Plaques of Carotid Artery
From the Department of Surgery, Oulu University Hospital (M.M., T.J.), National Public Health Institute, Department of Oulu (A.L., P.S., H.-M.S.), and Department of Microbiology, University of Oulu (R.K.), Oulu, Finland; the Department of Infectious Disease Epidemiology (M.L.) and the Department of Obstetrics and Gynecology (J.P.), University of Helsinki, Helsinki, Finland; the Department of Internal Medicine (J.J.), Kainuu Central Hospital, Kajaani, Finland; and the Department of Microbiology (R.P.M.), Montana State University, Bozeman.
Correspondence to Dr Tatu Juvonen, Department of Surgery, Oulu University Hospital, 90220 Oulu, Finland. E-mail tatu.juvonen{at}oulu.fi
Abstract—Linkage between Chlamydia pneumoniae infection and atherosclerosis has been confirmed in several studies, but the precise role of this organism in the disease process is not known. We investigated the relation and reactivity of T lymphocytes of human carotid plaques to C pneumoniae antigens. Tissue specimens were obtained from 17 patients who underwent carotid endarterectomy. Immunohistological staining and/or in situ hybridization revealed the presence of C pneumoniae in 11 (64%) of the 17 of the cases. Inflammatory infiltration seen in the vessel walls consisted primarily of CD45RO+ T-memory lymphocytes (median 80%, range 50% to 90%), whereas CD20+ B cells and monocytes were in minor proportion. In vivo activated T lymphocytes were propagated from the specimens with interleukin-2, and the antigen specificity of the established T-cell lines (TLLs) was analyzed against C pneumoniae elementary body antigen. TLLs were established from all 17 carotid tissues but none from the control specimens of ascending aorta. C pneumoniae was recognized as a specific T-cell–stimulating antigen in 7 (41%) of 17 cases. Further analyses of the C pneumoniae–reactive TLLs showed that chlamydial 60-kDa heat-shock protein induced specific proliferation in 5 (71%) of 7 cases and revealed 2 haplotype (DRB1*1502 and DQB1*06) binding motifs in human 60-kDa heat-shock protein. C pneumoniae was identified as a specific microbial antigen recognized by 41% of TLLs propagated from in vivo activated plaque T cells. Our results suggests that cell-mediated immunity to C pneumoniae plays a role in the atherosclerotic process and that this response may involve autoimmunity.
Key Words: atherosclerosis • Chlamydia pneumoniae • activated T cells
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