General agreement exists that in asthma, airway smooth muscle contracts, narrowing the airway lumen and thereby causing airflow obstruction and dyspnoea. New evidence is emerging that airway smooth muscle may also fulfil an immunomodulatory role by providing a rich source of pro-inflammatory cytokines and chemokines, polypeptide growth factors, extracellular matrix (ECM) proteins, cell adhesion receptors and co-stimulatory molecules. Together, the available data support a role for airway smooth muscle in actively perpetuating airway mucosal inflammatory processes including mast cell and leukocyte (T cell, neutrophil, eosinophil) activation and recruitment. Production of anti-inflammatory mediators by airway smooth muscle such as prostaglandin E(2) suggests that it is also capable of exerting a 'braking' effect on local inflammation. Recognition of this newly described property of airway smooth muscle makes it important to consider therapeutic targets for suppressing the synthesis and secretion of immunomodulatory mediators from this cell. However, it remains imperative to establish to what extent the secretory potential of airway smooth muscle is quantitatively important in vivo and in asthmatic subjects.