Background Surfactant protein A (SP-A) contributes to the regulation of sepsis-induced acute lung injury.In a previous study,we demonstrated the expression and localization of SP-A in the kidneys.The present study evaluated the effect of SP-A on lipopolysaccharide (LPS)-induced tumor necrosis factor-α (TNF-α) expression and its underlying mechanisms in the human renal tubular epithelial (HK-2) cells.Methods Indirect immunofiuorescence assay was used to detect SP-A distribution and expression in HK-2 cells.HK-2 cells were treated with various concentrations of LPS (0,0.1,1,2,5,and 10 mg/L) for 8 hours and with 5 mg/L LPS for different times (0,2,4,8,16,and 24 hours) to determine the effects of LPS on SP-A and TNF-α expression.Then,HK-2 cells were transfected with SP-A siRNA to analyze nuclear factor κB (NF-κB) P65 and TNF-α expression of HK-2 cells after LPS-treatment.Results Indirect immunofluorescence assay revealed that SP-A is localized to the membrane and cytoplasm of HK-2 cells.Interestingly,SP-A1/SP-A2 and TNF-α expression were found to be significantly increased in HK-2 cells upon LPS treatment.Transfection of LPS-treated HK-2 cells with SP-A siRNA resulted in significant increases in the levels of NF-κB P65 protein and TNF-α mRNA and protein compared to those in non-transfected LPS-treated HK-2 cells.Conclusion SP-A plays an important role in protecting cells against sepsis-induced acute kidney injury by inhibiting NF-κB activity to modulate LPS-induced increase in TNF-α expression.