Studies in asthma have confirmed that IgE is positively correlated with airway inflammation and remodeling, and its role in asthma is generally believed to be pleiotropic.[20–23] Studies with animal models demonstrated that the contact between airway epithelial cells and airborne allergens induced synthesis of IgE by increased production of IL-4 from lung cells, and IgE could further result in bronchitis and peribronchitis.[24–26] Studies by Vroling et al[27] and Tsai et al[28] indicate that the effect of allergy on airway inflammation in COPD is because of locally enhanced inflammation. This evidence concerns the gene IL4 and bronchitis.