Chlamydia pneumoniae and atherosclerosis. Identification of bacterial DNA in the arterial wall

Abstract

Objective -The intracellular Gram-negative bacterium Chlamydia pneumoniae has been associated with atherosclerosis. The presence of Chlamydia pneumoniae has been investigated in fragments of the arterial wall with a technique for DNA identification. Methods -Atherosclerosis and its associated diseases (acute myocardial infarction and ischemic stroke) are important causes of morbidity and mortality in industrialized and developing countries. Differences in the prevalence of conventional risk factors (smoking, hypertension, and dyslipidemia), however, do not explain temporal and geographic variations in the prevalence and severity of these diseases. About one third of the individuals with atherosclerosis are estimated not to have any of these major risk factors. This resulted in the search for new risk factors, such as coagulation factors, inflammatory factors, and infectious agents.Atherosclerosis is an inflammatory disease 1 . According to the current theory of atherogenesis, this process begins with an "initial injury" that triggers an inflammatory response involving lymphocytes, macrophages, smooth muscle cells, and endothelial cells. Some of the triggers proposed for the initial injury in atherosclerosis include the following: carbon monoxide of cigarettes, hemodynamic friction upon the endothelium, hypercholesterolemia, oxidized LDL, and more recently, infectious agents such as herpesvirus, cytomegalovirus, Helicobacter pylori, and Chlamydia pneumoniae.The association of Chlamydia pneumoniae and coronary, carotid, and peripheral arterial disease has been described in several countries in diverse types of studies as follows: a) serum-epidemiological studies 2-6 ; b) anatomicopathological studies 7-17 ; and c) experimental studies [18][19][20][21][22] . Reports on cultivation of Chlamydia pneumoniae in fragments of arteries exist, showing the viability of the bacterium and its multiplication capacity in that type of environment 10,12 . In vitro studies have shown the ability of Chlamydia pneumoniae to infect smooth muscle cells, endothelial cells, and human macrophages [23][24][25] . Experiments in rabbits infected with Chlamydia pneumoniae showed the development of fatty streaks and lesions similar to atherosclerosis in the aorta 18 . When the animals were treated with macrolides, however, these lesions did not develop 26 . Preliminary clinical randomized trials 27,28 that still await confirmation support a causal relation between Chlamydia pneumoniae and coronary artery disease.