Objective: To investigate the role of protease-activated receptor 2 (PAR2) involved in epithelial-mesenchymal transition (EMT) of human bronchial epithelial (HBE) cells. Method: 16HBE cells were stimulated with various concentrations of tryptase (a nature agonist of PAR2). Cell migration and repair were assessed by transwell and scratch assay. Western blot was used to examine the expressions of EMT associated biomarkers including E-cadherin, N-cadherin and α-smooth muscle actin (α-SMA). DCFH-DA probe was employed to measure the generation of reactive oxygen species (ROS). The effects of N-acety-1-cysteine (NAC) on 16HBE induced by tryptase were also examined by transwell and scratch assay. Results: Tryptase dramatically promoted cell migration and repair with loss of E-cadherin and increase of N-cadherin and α-SMA in a dose-dependent manner (P<0.05). Tryptase enhanced generation of ROS in 16HBE cells, and this effect can be inhibited by PAR2 antagonist FSLLRY-NH2 (FS) (P<0.05). ROS scavenger N-acety-1-cysteine (NAC) significantly inhibited the EMT changes induced by tryptase (P<0.05). Conclusion: Activation of PAR2 triggered HBE EMT process via ROS signal, which highlights a potential target for the regulation of HBE phenotype shift involved in airway remodeling.