1. Increased bronchoconstrictor responses to contractile agonists and decreased dilator responses to beta-adrenoceptor agonists are characteristics of human asthma. One explanation for these features of asthma is that cytokines released in the asthmatic airway have direct effects on airway smooth muscle cells that alter their phenotype. 2. The present review summarizes data indicating that inflammatory cytokines, such as interleukin (IL)-1 beta and tumour necrosis factor-alpha, T helper (h) 1 cytokines, such as interferon-gamma, and Th2 cytokines, such as IL-13 and IL-5, have the capacity to enhance contractile responses and/or decrease relaxant responses of airway smooth muscle. These effects are observed in smooth muscle from human airways and airway smooth muscle of other species. 3. Understanding the mechanistic basis for the effects of these cytokines may prove to be an important step in improving the efficacy of beta-adrenoceptor agonists for the treatment of asthma.