Aims In order for Chlamydia pneumoniae to play a causative role in chronic human disease, it would need to persist within infected tissue for extended periods of time. Current theory suggests that C pneumoniae may persist at the site of infection via an alternative replicative form, known as an aberrant body.
Methods A panel of C pneumoniae-specific antibodies upregulated by the aberrant body was used to probe tissue specimens from the coronary atheroma from 13 explanted hearts to identify patterns of reactivity in these tissues, as well as to determine the presence and prevalence of C pneumoniae aberrant bodies.
Results Six of 13 patients had an ischaemic cardiomyopathy secondary to coronary atherosclerosis, while another six patients had an idiopathic, dilated cardiomyopathy. One additional patient, a young (24 years) woman with cardiomyopathy, had no history of atherosclerotic disease. Eleven patients were positive by immunohistochemistry with at least one antibody. Coronary arteries of the two other patients were negative by immunohistochemistry with all antibodies. One of these patients was the 24-year-old woman with grade I disease and no risk factors for coronary artery disease.
Conclusions The protein antigens of persistent C pneumoniae infection found in the atheromatous lesions from patients in this study could potentially be used as markers to detect such infections and some may be virulence factors or immunogens specific to C pneumoniae, thus serving as target molecules for diagnostic use or therapeutic intervention.
- Chlamydia pneumoniae
- coronary atheroma
- heart transplantation
- virulence factors
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Collaborating investigators: R Nakamatsu, M Allen, F Arnold and P Peyrani, University of Louisville, Louisville, Kentucky; D Ackermann, Department of Pathology, Jewish Hospital, Louisville, Kentucky; G Zhong, University of Texas, San Antonio, Texas; P Timms, W Huston, Queensland University of Technology, Brisbane, Australia; U Ziegler, University of Zurich, Zurich, Switzerland; S von Aulock, University of Konstanz, Konstanz, Germany; C Kaiser, L Nufer, Institute of Veterinary Pathology, University of Zurich, Switzerland.
Funding This study was supported by grants from the American Heart Association (JTS) and the Bodenseehochschulförderung (NB, AP, SvA, CH, SB). Grant number AHA 0755338B, IBH 530/08.
Competing interests None.
Patient consent Obtained.
Ethics approval This study was approved by the University of Louisville Institutional Review Board.
Provenance and peer review Not commissioned; externally peer reviewed.
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