Eosinophil adhesion receptors.

Eosinophilic inflammation is often characterized by a paucity of tissue neutrophils. A possible explanation of this selective accumulation is utilization of different adhesion pathways by the two cell types. Eosinophil adhesion in vitro to unstimulated HUVEC is selectively enhanced by IL-5 and IL-3. This pathway appears to be Mac-1 dependent. At sites of chronic inflammation an array of adhesion molecules are likely to be induced on venular endothelium. Eosinophils, like other leukocytes, can potentially utilize all three selectin adhesion receptors as well as the immunoglobulin family member ICAM-1. In addition, unlike neutrophils, eosinophils express VLA-4 and can use the VLA-4/VCAM-1 pathway. In vitro IL-4 selectively upregulates VCAM-1 on HUVEC and promotes eosinophil transmigration via VCAM-1. However, bronchial biopsies of both asthmatics and controls revealed strong expression of E-selectin and ICAM-1 with very weak expression of VCAM-1. This would suggest that, despite the in vitro findings, VCAM-1 is not involved in eosinophil migration into the airways in chronic asthma.