학술논문
Persistent Chlamydia pneumoniae infection of cardiomyocytes is correlated with fatal myocardial infarction.
Document Type
Academic Journal
Author
Spagnoli LG; Cattedra di Anatomia ed Istologia Patologica, Dipartimento di Biopatologia e Diagnostica per Immagini, Università di Roma Tor Vergata, Via Montpellier 1, Rome, Italy. spagnoli@uniroma2.it; Pucci S; Bonanno E; Cassone A; Sesti F; Ciervo A; Mauriello A
Source
Publisher: Elsevier Country of Publication: United States NLM ID: 0370502 Publication Model: Print Cited Medium: Print ISSN: 0002-9440 (Print) Linking ISSN: 00029440 NLM ISO Abbreviation: Am J Pathol Subsets: MEDLINE
Subject
Language
English
ISSN
0002-9440
Abstract
Acute myocardial infarction (AMI) associated with unfavorable prognosis is likely to be the consequence of a diffuse active chronic inflammatory process that destabilizes the whole coronary tree and myocardium, suggesting a possible common causal agent underlying both conditions. The main objective of this study was to investigate whether Chlamydia pneumoniae (CP) infection occurred beyond the coronary plaques, namely in the myocardium of individuals who died of AMI. The presence of CP cell wall antigen (OMP-2) and CP-HSP60 was investigated in the myocardium and coronary plaques of 10 AMI and 10 age-matched control patients by immunohistochemistry, electron microscopy, and molecular biology. OMP-2 antigens were found in the unaffected myocardium of 9 of 10 AMI patients. Conversely, only 1 of 10 control patients exhibited a positive staining for CP. Moreover, OMP-2 and CP-HSP60 were detected in the whole coronary tree. CP presence was strongly associated with a T-cell inflammatory infiltrate. Our results suggest that CP may underlie both coronary and myocardial vulnerabilities in patients who died of AMI and corroborate the notion that CP may act by reducing cardiac reserves, thus worsening the ischemic burden of myocardium.