The present study, therefore, was designed to determine, using H2O2 and an experimental viral infection model, the following: (1) whether oxidative stress potentiates IL-33 expression in human airway epithelial cells and which signal pathways participate in the regulating mechanisms; (2) whether oxidative stress augments IL-33 expression in the dsRNA-treated or viral infected cells; and (3) whether antioxidant treatment decreases the expression of IL-33 in airway epithelial cells from COPD patients. Here, IL33 is linked to chronic obstructive pulmonary disease.