Premium
Ligand density modulates eosinophil signaling and migration
Author(s) -
Holub A.,
Byrnes J.,
Anderson S.,
Dzaidzio L.,
Hogg N.,
Huttenlocher A.
Publication year - 2003
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0502264
Subject(s) - biology , eosinophil , microbiology and biotechnology , ligand (biochemistry) , signal transduction , immunology , computational biology , receptor , biochemistry , asthma
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.