In order to investigate the roles and mechanisms of liver X receptor alpha (LXRα)-ATP binding cassette transporter A1 (ABCA1) pathway in Chlamydia pneumoniae (C. pneumoniae) infection induced macrophage lipid accumulation. THP-1 macrophage derived foam cells were used as the cell model. Cellular cholesterol was determined by high performance liquid chromatography analysis. Cholesterol efflux was determined by liquid scintillator. ABCA1 and LXRα mRNA expression was detected by RT-PCR and protein expression was detected by Western blot. Furthermore, we pretreated the cells with LXRα specific agonist T0901317, and then observed the changes of indexes mentioned above. The result showed that C. pneumoniae infection could increase the content of total cholesterol, free cholesterol and cholesterol ester, inhibit the efflux of cholesterol from cells, and reduce the expression of ABCA1 and LXRα. The suppression of C. pneumoniae infection on ABCA1 expression was significantly attenuated after the use of ABCA1 agonist 8-Br-cAMP or LXR agonist T0901317, correspondingly, cholesterol efflux was promoted and the content of intracellular cholesterol was elevated. These results suggested that the mechanism of C. pneumoniae infection promoting lipid accumulation in macrophages and suppresses cholesterol efflux may be related to LXRα-ABCA1 pathway.