Microbial Agents, Immune Function and Atheromatosis: The Chlamydophila pneumoniae Role

Some pathogens have been associated with the pathogenesis of atherosclerosis. The best studied and characterized has been Chlamydophila pneumoniae. Over the last years, several reports in the literature have suggested that infection with C. pneumoniae may contribute to the pathogenesis of atherosclerosis. C. pneumoniae would need to persist within infected tissue for extended periods of time, thereby stimulating a chronic inflammatory response. C. pneumoniae has been shown to disseminate systemically from the lungs and alveolar macrophages through infected peripheral blood mononuclear cells and to localize in arteries where it may infect incipient atheromatous lesions and their cellular compounds (endothelial cells, vascular smooth muscle cells (SMC), monocytes/macrophages). This situation promotes inflammatory atherogenous process. The involvement of C. pneumoniae in atherosclerosis was investigated by seroepidemiological and pathological studies, in vivo and in vitro studies, and in clinical antibiotic treatment trials. C. pneumoniae has been demonstrate in atheromas by inmunohistochemical techniques, DNA isolation and even has been cultured from arterial walls. The immune system may interplay between C. pneumoniae infection and coronary artery disease. Major histocompatibility complex genes regulate innate and adaptive immunity. A recent analysis showed the HLA-B35 allele to be the strongest-risk gene for C. pneumoniae infection.