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Journal of Clinical Microbiology, April 1999, p. 1013-1017, Vol. 37, No. 4
0095-1137/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Coronary Angioplasty Induces Rise in Chlamydia pneumoniae-Specific Antibodies

Andreas Tiran,1,* Rene A. Tio,2 Jacobus M. Ossewaarde,3 Beate Tiran,4 Peter den Heijer,2 T. Hauw The,5 and Martie M. Wilders-Truschnig1

Department of Laboratory Medicine1 and Institute of Medical Biochemistry,4 University of Graz, A-8010 Graz, Austria, and Department of Cardiology2 and Department of Clinical Immunology,5 University of Groningen, 9713 GZ Groningen, and Research Laboratory for Infectious Diseases, National Institute of Public Health and the Environment, 3720 BA Bilthoven,3 The Netherlands

Received 7 July 1998/Returned for modification 10 November 1998/Accepted 7 January 1999

Chlamydia pneumoniae is frequently found in atherosclerotic lesions, and high titers of specific antibodies are associated with increased risk for acute myocardial infarction. However, a causative relation has not been established yet. We performed a prospective study of 93 patients undergoing percutaneous transluminal coronary angioplasty (PTCA) to investigate whether angioplasty influences Chlamydia-specific antibody titers and whether there is an association with restenosis. Blood samples were obtained before and 1 and 6 months after angioplasty. Antibodies against chlamydial lipopolysaccharide and against purified C. pneumoniae elementary bodies were measured by enzyme-linked immunosorbent assay (ELISA). After angioplasty, the prevalence of antibodies to lipopolysaccharide rose from 20 to 26% for immunoglobulin A (IgA), from 53 to 64% for IgG, and from 2 to 7% for IgM (P = 0.021, 0.004, and 0.046, respectively). There was a rapid increase of mean antibody titers of all antibody classes within 1 month of PTCA. During the following 5 months, antibody titers decreased slightly but were still higher than baseline values. Results of the C. pneumoniae-specific ELISA were essentially the same. The rise of anti-Chlamydia antibodies was not caused by unspecific reactivation of the immune system, as levels of antibodies against cytomegalovirus did not change. Neither seropositivity nor antibody titers were related to restenosis. However, increases in mean IgA and IgM titers were restricted to patients who had suffered from myocardial infarction earlier in their lives. In conclusion, we show that PTCA induces a stimulation of the humoral immune response against C. pneumoniae. These data support the idea that plaque disruption during angioplasty might make hidden chlamydial antigens accessible to the immune system.

* Corresponding author. Mailing address: Department of Laboratory Medicine, University of Graz, Auenbruggerplatz 15, A-8010 Graz, Austria. Phone: 43 (316) 385-3239. Fax: 43 (316) 385-3430. E-mail: andreas.tiran{at}kfunigraz.ac.at.

Journal of Clinical Microbiology, April 1999, p. 1013-1017, Vol. 37, No. 4
0095-1137/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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