Chlamydia, inflammation, and atherogenesis

Atherosclerotic lesions are initiated and progress largely as a result of a chronic, fibroproliferative, inflammatory response. This review discusses how Chlamydia pneumoniae could conceivably contribute to this chronic infla mmatory response and reports on recent in vivo and in vitro studies. In viv o studies in mice demonstrate that C. pneumoniae infection is disseminated to the artery wall following infection in the lung by alveolar macrophages. Recent in vitro studies show that infected U937 cells can directly transfe r infection to endothelial cells and can indirectly increase the susceptibi lity of endothelial cells to C. pneumoniae infection. Loading of RAW 264.7 cells with modified forms of low-density lipoprotein increases the resistan ce of the cells to C. pneumoniae infection and also increases the susceptib ility to the combined toxic effects of modified lipids and C. pneumoniae in fection.