Chlamydia pneumoniae disrupts lipid metabolism in human umbilical vein endothelial cells

Atherosclerosis is well established as a chronic inflammatory disorder, and Chlamydia pneumoniae is considered to be a risk factor for atherosclerotic development. Endothelial dysfunction, caused by oxidized low-density lipoprotein (ox-LDL) is an early atherosclerotic marker. However, the effect of C. pneumoniae on lipid metabolism in vascular endothelial cells is yet to be elucidated. The aim of the present study was to investigate the effects of C. pneumoniae on lipid metabolism in human umbilical vein endothelial cells (HUVECs). In the present study, LDL oxidation was found to be significantly induced in the supernatant, but not the cell lysates, of C. pneumoniae-infected HUVECs. Furthermore, C. pneumoniae infection was observed to increase the levels of total cholesterol and cholesteryl esters in LDL-treated HUVECs. In addition, C. pneumoniae was found to upregulate the expression of scavenger receptor A, cluster of differentiation 36 and acyl-coenzyme A: cholesterol acyltransferase 1 mRNA and protein. C. pneumoniae Was also observed to downregulate the mRNA and protein expression of ATP binding cassette transporter (ABC) A1 and ABCG1 in LDL-treated HUVECs. These results show that C. pneumoniae disrupts lipid metabolism in HUVECs.