The epithelial-mesenchymal transition (EMT) plays significant role in airway remodeling during chronic obstructive pulmonary disease (COPD) and lung cancer. Aspirin-triggered resolvin D1 (AT-RvD1) presents anti-inflammatory and pro-resolution effects, via lipoxin A4 receptor/formyl peptide receptor 2 (ALX/FPR2). In addition, AT-RvD1 prevented TGF-β1-induced EMT in lung cancer cells (A549 cells). Here, we extend these results and evaluated the role of AT-RvD1 in cigarette smoke extract (CSE)-induced EMT on bronchial epithelial cells (BEAS-2B). CSE decreased E-cadherin expression, an epithelial marker, and increased ROS and TGF-β1 productions, and expressions of mesenchymal markers (N-cadherin, vimentin, smad2/3 and slug). Furthermore, CSE induced an increase in the ALX/FPR2 receptor expression. AT-RvD1 restored the expression of E-cadherin and reduced the N-cadherin, Vimentin, smad2/3 and ALX/FPR2 expressions as well as ROS and TGF-β1 productions on CSE-stimulated cells. In conclusion, AT-RvD1 has the potential to control epithelial-mesenchymal transition induced by smoking in the normal lung epithelial cells.