Chlamydia pneumoniae and atherosclerotic disease <b>[Abstract in English]</b>

Abstract

AIMS: To study the etiopathogenic role of Chlamydia pneumoniae infection in the atherosclerotic disease, in vitro studies and animal models involving Chlamydia pneumonia and atheromatosis were reviewed, as well as clinical assays that analyzed the association between the pathogen and atherosclerotic disease. SOURCE OF DATA: Articles found in Pubmed, SciELO and LILACS data bases, published between 1986 and 2009, were reviewed. SUMMARY OF FINDINGS: Chlamydia pneumoniae can replicate in the endothelium, smooth muscle cells and macrophages, contributing to atherogenesis. Lipopolysacharides and heat-shock proteins originated from the pathogen can induce the formation of foam cells. In vitro, human macrophages infected by Chlamydia pneumoniae induce intracellular accumulation of lipids through a deregulation in the absorption of low-density lipoproteins. In animal models, the pathogen is found in atheroma of hyperlipemic animals, and murine macrophages adhere better to the endothelium when infected by Chlamydia pneumoniae. The sero-epidemiological studies are controversial in terms of the anti-Chlamydia pneumoniae antibody frequency in patients with atherosclerosis. In clinical studies, there is no unequivocal evidence of the benefit of antibiotics on the prognosis of the coronary arterial disease. The occurrence of the infection by Chlamydia pneumonia is not, up to date, a defined risk factor for atherosclerotic disease. CONCLUSIONS: Infection by Chlamydia pneumonia may constitute an important etiopathogenic finding in atheromatosis. However, the clinical relevance of this association, as shown in the epidemiologic and clinical studies herein reviewed , is yet uncertain.