Introduction: Bronchial asthma is a disease of complex aetiology characterized by both pathological and physiological abnormalities which lead to widespread but reversible airways obstruction. Pathologically, the airways exhibit evidence of mucosal oedema, damage to the respiratory bronchial epithelium and infiltration with large numbers of eosinophils, neutrophils and mononuclear cells [1, 2]. One of the cardinal features of asthma is an increased reactivity of the airways to specific and nonspecific bronchial provocation. Whilst the reasons for this increased airway reactivity have not yet been defined, there is evidence that many of the pathophysiological changes in asthma, which are tantamount to an inflammatory response, may be accounted for by the actions of released chemical mediators [3, 4]. This article reviews some of the recent advances made in this area, with particular emphasis on the likely roles of those mast cell-dependent mediators which are generated de novo after cell activation.

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