Molecular medicine reports

Chlamydia pneumoniae disrupts lipid metabolism in human umbilical vein endothelial cells.

PMID 24898283


Atherosclerosis is well established as a chronic inflammatory disorder, and Chlamydiaxa0pneumoniae 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.xa0pneumoniae 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.xa0pneumoniae 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.xa0pneumoniae‑infected HUVECs. Furthermore, C.xa0pneumoniae infection was observed to increase the levels of total cholesterol and cholesteryl esters in LDL‑treated HUVECs. In addition, C.xa0pneumoniae was found to upregulate the expression of scavenger receptorxa0A, cluster of differentiationxa036 and acyl‑coenzymexa0A:xa0cholesterol acyltransferasexa01 mRNA and protein. C.xa0pneumoniae was also observed to downregulate the mRNA and protein expression of ATP binding cassette transporter (ABC)xa0A1 and ABCGl in LDL‑treated HUVECs. These results show that C.xa0pneumoniae disrupts lipid metabolism in HUVECs.