Asthma is a disease characterized, in part, by reversible airflow obstruction, hyperresponsiveness and inflammation. Traditional concepts concerning airway inflammation have focused on leukocyte trafficking and on the effects of inflammatory mediators, cytokines and chemokines secreted by these cells. Airway smooth muscle, the major effector cell responsible for bronchomotor tone, has been thought of as a passive tissue that responds to neurohumoral control and inflammatory mediators. New evidence, however, suggests that airway smooth muscle may secrete cytokines and chemokines and express cell adhesion molecules that are important in modulating submucosal airway inflammation. The cellular and molecular mechanisms that regulate the immunomodulatory functions of airway smooth muscle may offer new and important therapeutic targets in treating this common lung disease.