Asthma is characterised by a 50-fold increase in the number of eosinophils relative to neutrophils in the bronchial mucosa. This is the result of the cumulative and sequential effects of several, approximately fourfold, increases in selective eosinophil versus neutrophil migration occurring at a number of stages in the life cycle of the eosinophil. These events, which are integrated and directed by allergen-specific T helper 2 lymphocytes through the generation of interleukin (IL)-5, IL-4 and

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... -13, include: effects on the bone marrow, mediated principally by IL-5, which result in a fourfold increase in circulating eosinophils selective tethering of eosinophils to venular endothelium through the combined effects of P-selectin/P-selectin glycoprotein ligand (PSGL)-1 and very late activation antigen (VLA)-4/vascular cell adhesion molecule-1, which has the potential for an up to tenfold increase in eosinophil versus neutrophil adhesion selective chemotaxis under the influence of CC chemokines prolonged survival, again mediated by IL-5. The implications of this multistep process are that antagonists of IL-5, VLA-4, PSGL-1 and CC chemokine receptor 3, as well as IL-4 and IL-13, each have the potential markedly to inhibit eosinophil recruitment in asthma.