As with other types of leukocytes, mechanisms that function to enable the recruitment of eosinophils into specific sites of immune reactions involve a complex and cumulative interplay of many molecules and pathways. No single chemoattractant is specific for eosinophils, but rather various chemoattractants active on eosinophils can also elicit migration of other specific cell types. Humoral mediators causing eosinophil migration include C5a and platelet-activating factor, whereas cytokines active as eosinophil chemoattractants include interleukin (IL)-2, IL-3, IL-5, granulocyte/macrophage colony-stimulating factor, lymphocyte chemoattractant factor, and RANTES. Eosinophils utilize several pathways to adhere to vascular endothelial cells, including binding to intercellular adhesion molecule-l, E-selectin, and vascular cell adhesion molecule-l (VCAM-1). The lack of binding of neutrophils to VCAM-1 and the enhanced expression of VCAM-l elicited by IL-4 contribute to preferential eosinophil accumulation. Eosinophil recruitment is dependent not only on ligands expressed on eosinophils and molecules inducible on endothelial cells but also on processes active during transendothelial migration and extravascular migration in the extracellular spaces.

Eosinophilic leukocytes are recruited into sites of early-and late-phase immediate hypersensitivity reactions as well as into tissue sites of other immunologically mediated diseases. The evidence for the contribution-of the eosinophil and eosinophil-elaborated mediators to the pathophysiology of these disorders is increasing (1). While eosinophils may be present to varying extents with other cell types, including neutrophils, lymphocytes, and monocytes, the mechanisms whereby eosinophils, a minority of circulating blood leukocytes, are recruited in large numbers into tissue sites have been uncertain. This predominant infiltration of eosinophils cannot be explained solely by the release of chemotactic factors such as C5a, platelet-activating factor (PAF), and leukotriene B4 (LTB4) as they are likewise active in neutrophil recruitment (2). Mobilization of eosinophils into the inflammatory site involves adhesion and transmigration through the endothelial barrier, a process that can be regulated by differential expression of adhesion molecules on both eo-