Objective To study the role of E-selection and macrophage inflammatory protein-2（MIP-2） in the airway inflammation in a rat model of chronic obstructive pulmonary disease（COPD）.Methods Twenty-four male SD rats were randomly divided into a normal control group and a COPD group.The rat model of COPD was established by exposure to cigarette smoking.Lung function，pathologic features of lung tissues and inflammatory cell differentials in bronchoalveolar lavage fluid（BALF） were investigated.Immunohistochemistry was employed to examine the expression of E-selection in lung tissue.The levels of MIP-2 in BALF，serum and lung tissues were measured with ELISA.Results The changes in histopathology and pathophysiology in the rat COPD model were similar to those in COPD patients.The expression of E-selection on bronchopulmonary vein endothelial cells of the COPD group significantly increased as compared with the normal control group（Plt;0.05） and was positively correlated with the neutrophil counts in BALF in the COPD group（ｒ=0.809，Plt;0.01）.The levels of MIP-2 in BALF and lung tissues in the rats with COPD were signicantly higher than those in normal rats，both of which were positively correlated with the neutrophil counts in BALF in the COPD group（r=0.893，Plt;0.01；r=0.716，Plt;0.05）.Conclusion Both E-selection and MIP-2 may be involved in the process of airway inflammation in COPD.