The pathologic manifestation of an allergic airway response is a culmination of several coordinated events involving the participation of multiple mechanisms and cell types. The early release of mast cell-derived arachidonic acid metabolites, production of early-response cytokines, and increased expression of adhesion molecules and production of chemokines all lead to the recruitment of multiple cell types with the ability to participate in the allergic airway response. The coordinated use of animal models related to clinical observations will allow further elucidation of the mechanisms involved in the initiation, maintenance, and regulation of allergic airway inflammation leading to airway damage.