The contractile capacity of airway smooth muscle is not fixed but modulated by an impressive number of extracellular inflammatory mediators. Targeting the transient component of airway hyperresponsiveness ascribed to this contractile lability of ASM is a quest of great promises in order to alleviate asthma symptoms during inflammatory flares. However, owing to the plethora of mediators putatively involved and the molecular heterogeneity of asthma, it is more likely that many mediators conspire to increase the contractile capacity of ASM, each of which contributing to a various extent and in a time-varying fashion in individuals suffering from asthma. The task of identifying a common mend for a tissue rendered hypercontractile by imponderable assortments of inflammatory mediators is puzzling.
Keywords: airway hyperresponsiveness; airway smooth muscle; asthma; contractile lability; inflammation.