The phagocytosis to Staphylococcus aureus (SA) and cultivated U937 cells by macrophages derived from PBMC was enhanced significantly under lipopolysaccharide(LPS) stimulation. The present experiment showed that the application polyclone antibodies to TLR2 suppressed partly the phagocytosis of macrophages in this model. The LPS-enhanced phagocytosis could be further blocked partly by polyclone antibodies to TRAIL or TNFα. Cells cultivated in a lower serum concentration(1%) was also shown to be a decreased phagocytosis. The results confirmed that TLR2 was a LPS receptor which mediated its signal transduction, while some serum factors participated in the binding of LPS to its membrane receptors. It further suggested that LPS induced effectors such as TRAIL and TNFα might be the key mediators involved in the mechanisms of LPS-enhanced phagocytosis.