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(Journal of Leukocyte Biology. 2003;73:657-664.)
© 2003 by Society for Leukocyte Biology

Ligand density modulates eosinophil signaling and migration

A. Holub*, J. Byrnes*, S. Anderson*, L. Dzaidzio*, N. Hogg{dagger} and A. Huttenlocher*

* Departments of Pediatrics and Pharmacology, University of Wisconsin, Madison; and
{dagger} Imperial Cancer Research Fund, Lincoln’s Inn Fields, London, United Kingdom

Correspondence: Anna Huttenlocher, Departments of Pediatrics and Pharmacology, University of Wisconsin Medical School, 3780 MSC, 1300 University Ave., Madison, WI 53706. E-mail: huttenlocher{at}facstaff.wisc.edu

Eosinophils are a major component of the inflammatory response in persistent airway inflammation in asthma. The factors that determine the retention of eosinophils in the airway remain poorly understood. Elevated levels of fibronectin have been observed in the airway of patients with asthma, and the levels correlate with eosinophil numbers. To determine if fibronectin density modulates eosinophil function, we investigated the effect of fibronectin and vascular cell adhesion molecule 1 (VCAM-1) density on eosinophil migration and signaling via the p38 and extracellular regulated kinase (ERK)–mitogen-activated protein kinase (MAPK) signaling pathways. There was a dose-dependent inhibition of eosinophil spreading and migration on increasing concentrations of fibronectin but not VCAM-1. In addition, activation of p38 MAPK was inhibited at high fibronectin but not high VCAM-1 concentrations, and ERK activity was slightly reduced at high VCAM-1 and fibronectin concentrations. Together, the results demonstrate that fibronectin but not VCAM-1 inhibits eosinophil migration and signaling.

Key Words: fibronectin • VCAM • motility • p38 MAPK




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