Exposure to Chlamydia pneumoniae is extremely common, and
respiratory infections occur repeatedly among most people. Strong associations exist between C. pneumoniae
infection and
atherosclerosis as demonstrated by: (i) sero-epidemiological studies showing that patients with
cardiovascular disease have higher titres of anti-C. pneumoniae
antibodies compared with control patients; (ii) detection of the organism within atherosclerotic lesions, but not in adjacent normal tissue by immunohistochemistry, polymerase chain reaction and electron microscopy and by culturing the organism from lesions; and (iii) showing that C. pneumoniae can either initiate lesion development or cause exacerbation of lesions in rabbit and mouse animal models respectively. The association of this organism with
atherosclerosis has also provided sufficient impetus to conduct a variety of human
secondary prevention antibiotic treatment trials. The results of these studies have been mixed and, thus far, no clear long-lasting benefit has emerged from these types of investigations. Studies of C. pneumoniae pathogenesis have shown that the organism can infect many cell types associated with both respiratory and cardiovascular sites, including lung epithelium and resident alveolar macrophages, circulating monocytes, arterial smooth muscle cells and vascular endothelium. Infected cells have been shown to exhibit characteristics associated with the development of
cardiovascular disease (e.g. secretion of proinflammatory
cytokines and procoagulants by infected endothelial cells and foam cell formation by infected macrophages). More detailed analysis of C. pneumoniae pathogenesis has been aided by the availability of genomic sequence information. Genomic and proteomic analyses of C. pneumoniae
infections in relevant cell types will help to define the pathogenic potential of the organism in both respiratory and
cardiovascular disease.