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Research Article Free access | 10.1172/JCI2688

The C-C chemokine receptor CCR3 participates in stimulation of eosinophil arrest on inflammatory endothelium in shear flow.

J Kitayama, C R Mackay, P D Ponath, and T A Springer

Center for Blood Research and Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.

Find articles by Kitayama, J. in: PubMed | Google Scholar

Center for Blood Research and Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.

Find articles by Mackay, C. in: PubMed | Google Scholar

Center for Blood Research and Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.

Find articles by Ponath, P. in: PubMed | Google Scholar

Center for Blood Research and Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.

Find articles by Springer, T. in: PubMed | Google Scholar

Published May 1, 1998 - More info

Published in Volume 101, Issue 9 on May 1, 1998
J Clin Invest. 1998;101(9):2017–2024. https://doi.org/10.1172/JCI2688.
© 1998 The American Society for Clinical Investigation
Published May 1, 1998 - Version history
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Abstract

Chemokines are widely hypothesized to stimulate firm adhesion of leukocytes on endothelium in shear flow. Thus far, this has been demonstrated experimentally for exogenously added chemoattractants, but not for those released by endothelium. We found that human umbilical cord endothelial cells (HUVEC) stimulated with TNF-alpha and IFN-gamma secreted eosinophil chemoattractants into the culture supernatant. This material induced transendothelial chemotaxis, stimulated eosinophil binding to purified intercellular adhesion molecule 1, and augmented binding to purified vascular cell adhesion molecule 1 in a 3-min static assay. Chemotaxis and stimulation of adhesion were abrogated completely by the pretreatment of eosinophils with an mAb to the C-C chemokine receptor 3 (CCR3). Eosinophils accumulated efficiently on HUVEC stimulated with TNF-alpha and IFN-gamma in shear flow at 1.5 dyn/cm2. CCR3 mAb slightly but significantly reduced eosinophil arrest and accumulation, by preventing development of firm adhesion by some of the tethered eosinophils, so that they detached within 30 s after the initial tethering. In the presence of mAb to the alpha4 integrin subunit, the effect of CCR3 mAb was more prominent, and approximately half of eosinophil arrest and accumulation was abolished. Inhibition by CCR3 mAb in the presence of beta2 integrin mAb was similar to that in control eosinophils. This is the first evidence that endothelial cell-derived chemokines can activate firm adhesion through alpha4 and beta2 integrins even in the presence of shear flow.

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