MEI Chun-Li, HE Ping, CHENG Bei, LIU Wei, WANG Yan-Fu, and WAN Jing-Jing
Department of Gerontology, Union Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China 在知网中查找 在百度中查找 在本站中查找
Aim To investigate the mechanisms of chlamydia pneumoniae (Cpn)-induced human monocytic cell line (THP-1)-derived foam cell formation, the expression of scavenger receptor A (SR-A1) and CD36 were examined. Methods THP-1-derived macrophages were incubated with or without increasing concentrations of Cpn (1×105 to 1×106 IFU) for 0 to 72 h. Lipid droplets in cytoplasm were observed by oil red O staining. The contents of intracellular cholesterol ester were detected by enzyme-fluorescence. The expression of SR-A1 and CD36 at mRNA and protein levels were determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western-Blot, respectively. Results Higher concentrations of Cpn infection (5×105 and 1×106 IFU) for 48 h result in the large accumulation of lipid droplets and the ratio of cholesteryl ester to total cholesterol was much higher than 50% in THP-1-derived macrophages when co-cultured with low density lipoprotein (LDL). Although Cpn infection had no effect on CD36 mRNA and protein expression, it up-regulated the expression of SR-A1 mRNA and protein in concentration-and time-dependent manner in THP-1 macrophages when co-cultured with LDL. Conclusions Cpn induces THP-1-derived foam cell formation by up-regulating the expression of SR-A1, which may provide a new evidence for the development and progression of atherosclerosis initiated by Cpn infection.