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.