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Thromboxane A2

rapidly. Readers are directed to excellent review articles [48,49]. Mediators, thus released, exert potent biological actions that include airway smooth muscle contraction, increased capillary permeability (to result in mucosal edema), increased epithelial permeability, mucus secretion, inflammatory cell chemotactic activity, and increased airways responsiveness, i.e., their actions are proinflammatory. Other stimuli in addition to specific antigen may also educe the release of mediators from inflammatory cells, some of these are shown in Fig. 3.

In the treatment of airways diseases involving mediator release, therapeutic interventions have been directed at: (1) inhibition of mediator release or synthesis or (2) inhibition of the biological actions of released mediators. Should mediator release or the resultant inflammatory state be responsible for induction of airway hyperreactivity, it would be expected that these same therapeutic interventions would be beneficial in returning the airway reactivity of asthmatics toward that of nonasthmatic individuals.

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