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Dissection of the Hyperadhesive Phenotype of Airway Eosinophils in Asthma

Department of Biomolecular Chemistry, and Department of Medicine, University of Wisconsin–Madison, Madison, Wisconsin

Correspondence and requests for reprints should be addressed to Deane F. Mosher, Department of Medicine, University of Wisconsin-Madison, 4285A Medical Sciences Center, 1300 University Avenue, Madison, WI 53706-1532. E-mail: dfmosher{at}facstaff.wisc.edu

Asthma is characterized by appearance of eosinophils in the airway. Eosinophils purified from the airway 48 h after segmental antigen challenge are described as exhibiting greater adhesion to albumin-coated surfaces via an unidentified 2 integrin and increased expression of M2 (CD11b/18) compared with purified blood eosinophils. We have investigated the determinants of this hyperadhesive phenotype. Airway eosinophils exhibited increased reactivity with the CBRM1/5 anti-M activation-sensitive antibody as well as enhanced adhesion to VCAM-1 (CD106) and diverse ligands, including albumin, ICAM-1 (CD54), fibrinogen, and vitronectin. Purified blood eosinophils did not adhere to the latter diverse ligands. Enhanced adhesion of airway eosinophils was blocked by anti-M2. Podosomes, structures implicated in cell movement and proteolysis of matrix proteins, were larger and more common on airway eosinophils adherent to VCAM-1 when compared with blood eosinophils. Incubation of blood eosinophils with IL-5 replicated the phenotype of airway eosinophils. That is, IL-5 enhanced recognition of M by CBRM1/5; stimulated M2-mediated adhesion to VCAM-1, albumin, ICAM-1, fibrinogen, and vitronectin; and increased podosome formation on VCAM-1. Thus, the hyperadhesion of airway eosinophils after antigen challenge is mediated by upregulated and activated M2.

Key Words: adhesion molecules • cell trafficking • eosinophils • human

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