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Infect Immun, April 1998, p. 1370-1376, Vol. 66, No. 4
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Characterization of a Strain of Chlamydia pneumoniae Isolated from a Coronary Atheroma by Analysis of the omp1 Gene and Biological Activity in Human Endothelial Cells

Robert E. Molestina,1,2 Deborah Dean,3 Richard D. Miller,2 Julio A. Ramirez,1 and James T. Summersgill1,2,*

Division of Infectious Diseases, Department of Medicine,1 and Department of Microbiology and Immunology,2 University of Louisville School of Medicine, Louisville, Kentucky, and Division of Infectious Diseases, Department of Medicine, and the Francis I. Proctor Foundation, University of California San Francisco School of Medicine, San Francisco, California3

Received 19 November 1997/Returned for modification 5 January 1998/Accepted 15 January 1998

Chlamydia pneumoniae is a respiratory pathogen that has been associated with chronic inflammatory diseases such as asthma and atherosclerosis. Recent isolation of C. pneumoniae from human carotid and coronary atheromas provides additional support for a role of this organism in atherogenesis. We characterized the coronary strain C. pneumoniae A-03 by sequence analysis of the major outer membrane protein gene (omp1). In addition, the in vitro activities of A-03 and three respiratory strains of C. pneumoniae (BAL-16, TW-183, and T-2634) were examined in infected human umbilical vein endothelial cells (HUVEC) by analysis of the production of interleukin-8 (IL-8), monocyte chemotactic protein 1 (MCP-1), and soluble intercellular cell adhesion molecule 1 (sICAM-1). Sequence analysis of omp1 of C. pneumoniae A-03, compared to prototype strains TW-183 and AR-39, revealed five nucleotide changes resulting in nonsynonymous codons. Of interest was a nonconservative amino acid substitution (Ser to Pro) in position 61 of variable segment 1. In vitro, the extent of MCP-1, IL-8, and sICAM-1 production was dependent on the C. pneumoniae strain examined at low multiplicities of infection following 24 h of incubation. Strain A-03 displayed the lowest stimulatory activity in infected HUVEC, while T-2634 induced the highest levels of MCP-1, IL-8, and sICAM-1 among all strains examined. Heat-inactivated C. pneumoniae failed to stimulate production of these proteins by all strains tested. In contrast, only partial inhibition was observed by UV-inactivated organisms. Results from this study demonstrate that unlike prototype respiratory strains of C. pneumoniae, the coronary strain A-03 displays divergence in the omp1 gene. In addition, the stimulation of chemokines and adhesion molecules involved in the recruitment of leukocytes to sites of inflammation by C. pneumoniae may be important in the pathogenesis of diseases associated with this organism, including atherosclerosis.

* Corresponding author. Mailing address: Division of Infectious Diseases, MDR Building, Room 622, Department of Medicine, University of Louisville, Louisville, KY 40292. Phone: (502) 852-5132. Fax: (502) 852-1147. E-mail: JTSUMM01{at}ulkyvm.louisville.edu.




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