Previous studies have shown that lipopolysaccharide (LPS) induces acute lung injury (ALI), and that endothelial progenitor cells (EPCs) participate in tissue repair. Therefore, in this study it was hypothesized that LPS influences the number and function of EPCs directly. In order to investigate this, an in vitro study was performed using EPCs. EPCs were cultured for seven days (early EPCs), and then treated with increasing concentrations of LPS (10 pg/ml, 100 pg/ml, 1 ng/ml, 10 ng/ml and 100 ng/ml) for 4, 8, 12, and 24 h. The proliferation, senescence and adhesion of EPCs was then assessed. Alongside this an in vivo study was also performed. Mice were administered LPS (2.5 mg/kg) via the trachea. After 4, 8, 12, and 24 h, EPCs were harvested and cultured for seven days, and the proliferation, senescence and adhesion of the EPCs were examined. The results showed that the rate of adhesion and senescence of EPCs decreased in vitro when treated with 10 and 100 ng/ml LPS. The adhesion and senescence rate also decreased after 12 and 24 h in vivo. Proliferation, however, was increased in vitro following treatment with 10 and 100 ng/ml LPS, but proliferation in vivo decreased after 8 and 12 h. The effects of LPS on EPCs were distinct in vivo and in vitro. In vitro, cells were sensitive to 100 ng/ml LPS. In the course of ALI induced by LPS, the proliferation and adhesion activity of the EPCs was activated in 8 h and then gradually decreased with time.