Chlamydia pneumoniae and atherosclerosis: current state and future prospectives.

Chlamydia pneumoniae, an intracellular bacterial pathogen, is known as a leading cause of human respiratory tract infections worldwide. Over the last decade, several reports in the literature have suggested that infection with C. pneumoniae may contribute to the pathogenesis of atherosclerosis. In order to playa causative role in chronic disease, C. pneumoniaewould need to persist within infected tissue for extended periods of time, thereby stimulating a chronic inflammatory response. C. pneumoniaehas been shown to disseminate systemically from the lungs through infected peripheral blood mononuclear cells and to localize in arteries where it may infect endothelial cells, vascular smooth muscle cells, monocytes/macrophages and promote inflammatory atherogenous process. The involvement of C. pneumoniaein atherosclerosis was investigated by seroepidemiological and pathological studies, in vivo and in vitro studies, and in clinical antibiotic treatment trials. This review will provide an update on the role of C. pneumoniaein atherosclerosis focusing on the recent insights and suggesting areas for future research.