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Published ahead of print on April 6, 2006, doi:10.1165/rcmb.2006-0027OC

Am. J. Respir. Cell Mol. Biol., Volume 35, Number 3, September 2006, 378-386

A more recent version of this article appeared on September 1, 2006
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Submitted on January 23, 2006
Revised on April 5, 2006

Dissection of the Hyper-adhesive Phenotype of Airway Eosinophils in Asthma

Steven R Barthel1, Nizar N Jarjour2, Deane F Mosher1*, and Mats W Johansson2

1 Department of Biomolecular Chemistry, University of Wisconsin-Madison, Madison, WI, USA; Department of Medicine, University of Wisconsin-Madison, Madison, WI, USA, 2 Department of Medicine, University of Wisconsin-Madison, Madison, WI, USA

* To whom correspondence should be addressed. E-mail: dfmosher{at}facstaff.wisc.edu.

Asthma is characterized by appearance of eosinophils in the airway. Eosinophils purified from the airway 48 hours after segmental antigen challenge are described as exhibiting greater adhesion to albumin-coated surfaces via an unidentified {beta}2 integrin and increased expression of {alpha}M{beta}2 (CD11b/18) in comparison to purified blood eosinophils. We have investigated the determinants of this hyper-adhesive phenotype. Airway eosinophils exhibited increased reactivity with the CBRM1/5 anti-{alpha}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-{alpha}M{beta}2. 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 to blood eosinophils. Incubation of blood eosinophils with IL-5 replicated the phenotype of airway eosinophils. That is, IL-5 enhanced recognition of {alpha}M by CBRM1/5; stimulated {alpha}M{beta}2-mediated adhesion to VCAM-1, albumin, ICAM-1, fibrinogen, and vitronectin; and increased podosome formation on VCAM-1. Thus, the hyper-adhesion of airway eosinophils after antigen challenge is mediated by upregulated and activated {alpha}M{beta}2.




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