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*
Department of Medicine, Division of Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, MD 21224; and
Department of Chemical Engineering, Johns Hopkins University, Baltimore, MD 21218
Selective eosinophil recruitment is the result of orchestrated
events involving cell adhesion molecules, chemokines, and their
receptors. The mechanisms by which chemokines regulate eosinophil
adhesion and migration via integrins are not fully understood. In our
study, we examined the effect of CCR3-active chemokines on eosinophil
adhesion to VCAM-1 and BSA under both static and flow conditions. When
eotaxin-2 or other CCR3-active chemokines were added to adherent
eosinophils, it induced rapid and sustained eosinophil detachment from
VCAM-1 in a concentration-dependent manner. Adhesion was detectably
reduced within 3 min and was further reduced at 10–60 min.
Simultaneously, eotaxin-2 enhanced eosinophil adhesion to BSA.
Preincubation of eosinophils with the CCR3-blocking mAb 7B11 completely
prevented chemokine-induced changes in adhesion to VCAM-1 and BSA.
Using a different protocol, pretreatment of eosinophils with chemokines
for 0–30 min before their use in adhesion assays resulted in
inhibition of VCAM-1 adhesion and enhancement of BSA adhesion. By flow
cytometry, expression of 
4 integrins and a
ß1 integrin activation epitope on eosinophils was
decreased by eotaxin-2. In a flow-based adhesion assay, eotaxin-2
reduced eosinophil accumulation and the strength of attachment to
VCAM-1. These results show that eotaxin-2 rapidly reduced
4 integrin function while increasing ß2
integrin function. These findings suggest that chemokines facilitate
migration of eosinophils by shifting usage away from ß1
integrins toward ß2 integrins.
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