Airway epithelial cells (ECs) form a continuous pseudostratified layer in the lung, creating a tight barrier that protects underlying tissue from the external environment. As such, airway ECs have been described classically as barrier cells that are involved in homeostasis; these cells respond to a variety of environmental stimuli, resulting in the alteration of their cellular functions, such as ion transport and movement of airway secretions. Recent evidence, however, suggests that airway ECs may also act as immune-effector cells, in response to noxious endogenous or exogenous stimuli. Several studies have shown that airway ECs express and secrete various immune molecules, such as lipid mediators, oxygen radicals, adhesion molecules, and a wide variety of cytokines, including chemokines (1). Through the expression and production of these immune molecules, the epithelium is now thought to be important in the initiation and exacerbation of inflammatory diseases of the lung, such as asthma.