*3.3.5 Chlamydia pneumoniae in the atherosclerotic plaque*

Many of previous studies including immunohistochemistry, polymerase chain reaction, and cultures demonstrated the presence of CP in various stages of human atheromatous plaques [21, 73, 74]. The existence of these bacteria in the atherosclerotic plaque can be explained by either direct infection of the vessel and/or transportation *via* circulating infected monocytes [69].

Although the exact mechanism with the atherosclerosis development is unclear, previous *in vitro* and animal studies have demonstrated the atherosclerosis relevant alterations triggered by the CP infections; the upregulation of the atherosclerosisrelated gene expression products in cultured cells such as the heat shock proteins 60 (HSP60), macrophage scavenger receptor, cytochrome p450, and VEGF165R; smooth muscle cell proliferation enhancement (mediated through platelet-derived growth factor); increased macrophage foam cell formation are some demonstrated examples of these modifications [71, 75–77].
