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Subsequent exposure of the same antigen to the cells of the airway epithelium initiates the acute phase reaction. IgE-studded mast cells of the airway degranulate causing release of vasoactive mediators such as histamine, increase the synthesis of prostaglandins and leukotrienes, and increase the transcription of cytokines. The mediators affect the bronchial mucosa by increasing mucosal edema, mucus production, smooth muscle constriction, and chemotactic factors which recruit other immune cells.