Bronchial asthma is considered to be a chronic airway inflammatory disease influenced by genetics and environmental factors. Airway hyperresponsiveness (AHR) is a characteristic of the disease generally associated with airway inflammation. Recently, the potential targets for therapeutic intervention in AHR has focused on the inhibition or antagonism of lipid mediators including leukotrienes, thromboxanes and platelet-activating factor. Furthermore, the inhibition of Th2 cytokines, such as interleukin-4 or interleukin-5, is another target for the prevention of AHR. In the present review, we describe the role of cytokines and arachidonic acid metabolites in the onset and development of AHR.