The role of Chlamydia pneumoniae in atherosclerosis – recent evidence from animal models

In summary, the cumulative evidence from animal models supports a pathogenic role for C. pneumoniae in atherosclerosis. The pathogenesis of the organism is consistent with it being at the site of lesion formation. In the mouse model, infected macrophages disseminate the infection and establish persistent infection of the aorta in foam cells within the atherosclerotic lesion11xMurine models of C. pneumoniae infection and atherosclerosis. Moazed, T.C. et al. J. Infect. Dis. 1997; 175: 883–890Crossref | PubMedSee all References, 12xSystemic dissemination of C. pneumoniae infection via macrophages. Moazed, T.C. et al. J. Infect. Dis. 1998; 177: 1322–1325Crossref | PubMedSee all References. This simulates human infection, in which the organism has also been found in foam cells2xCurrent knowledge on the association of Chlamydia pneumoniae and cardiovascular disease. Campbell, L.A. et al. Emerg. Infect. Dis. 1998; 4: 571–579Crossref | PubMedSee all References2. Lastly, there is evidence that C. pneumoniae infection can accelerate the progression of atherosclerosis in conjunction with hyperlipidemia and initiate histopathological changes in the aorta in mouse and rabbit models. Whether infection alone can induce definitive atherosclerosis needs to be further investigated.