Bronchial hyperresponsiveness is generally assessed by testing with methacholine (MCh) or histamine. Another possible stimulus with which to measure bronchial hyperresponsiveness is adenosine 5′-monophosphate (AMP). We have demonstrated previously1 that the provocative concentration of a substance (ie, AMP) causing a 20% fall in FEV1 (PC20) better reflects airway inflammation in asthma patients than does the MCh PC20. AMP, and by implication adenosine, acts by the release of a variety of inflammatory mediators from mast cells. We intended to assess with the study whether this AMP-induced mediator release initiates an inflammatory process resulting in the recruitment of eosinophils to the airways.