Abstract： Objective To explore the expression of intercellular adhesion molecule-1 (ICAM-1) in cultured human alveolar type 2 cells (A549) stimulated by mechanical force in vitro. Methods Cells were divided into 3 groups: a tensile stress group, a compressive stress group and a control group. The four-point bending system was used to stimulate A549 cells. The cells were stimulated by tensile stress or compressive stress respectively at the same magnitude of 1000 μstrain for 6 h. Sham cells in control group were not subjected to mechanical loading. The protein level and mRNA level of ICAM-1 were measured by Western blot and RT-PCR. Then an inhibitor was added to further explore the possible mechanism. The cells were divided into a tensile stress + inhibitor group, a compressive stress + inhibitor group and a control group. The cells were pretreated with PD98059, a specific inhibitor of extracellular signal-regulated kinase ( ERK) for 60 min, and then stimulated respectively by tensile stress or compressive stress at the same magnitude of 1000 μstrain for 6 h or were not subjected to mechanical loading. ICAM-1 protein and mRNA concentrations were determined by Western blot and RT-PCR, respectively. The data were analyzed by one-way ANOVA and Student-Newman-Keuls were used to compare 2 means. Results The expression of ICAM-1 protein in the tensile stress group ( 1. 16 ± 0.07) or the compressive stress group (1. 05 ± 0. 02) were significantly higher than that of the control group (0. 78 ± 0. 07, F = 3. 31, P < 0. 05 ) , and the expression of ICAM-1 mRNA in the tensile stress group (1.42 ±0. 05) or the compressive stress group (1. 27 ±0. 05) were also significantly higher than that of the control group ( 0. 13 ± 0. 04, F = 23. 1, P < 0. 01). After pretreated with PD98059 for 60 min, the expression of ICAM-1 protein in the tensile stress group (1.62 ±0.10) was significantly higher than that of the control group ( 0. 50 ± 0. 03, q = 3. 75, P < 0. 05 ) , while there was no significant difference between the compressive stress group (0. 60 ±0. 03, q =0. 32, P >0. 05) and the control group. At the transcription level, the expression of ICAM-1 in the tensile stress group (1.57 ±0.03) was significantly higher than that of the control group ( 0. 35 ± 0. 29, q = 3. 51, P < 0.05 ) , while there was no significant difference between the compressive stress group (0. 46 ±0. 03 , q =0. 32,P >0. 05) and the control group. Conclusions Mechanical forces upregulate the expression of ICAM-1 in A549 cells. PD98059 partly inhibits the upregulation of ICAM-1 induced by mechanical forces. ERK pathway may be partly involved in signal transduction of mechanical force induced expression of ICAM-1 in A549 cells.