Human eosinophil, but not neutrophil, adherence to IL-1-stimulated human umbilical vascular endothelial cells is alpha 4 beta 1 (very late antigen-4) dependent

G M Walsh, J J Mermod, A Hartnell, A B Kay, A J Wardlaw

Research output: Contribution to journalArticlepeer-review

254 Citations (Scopus)


Eosinophils, through their ability to generate an array of potent mediators, are thought to be the major effector cells in a number of conditions, including parasitic infection, asthma, and other allergic diseases. The mechanism(s) by which eosinophils, as opposed to neutrophils, accumulate at inflammatory sites is unknown. One possible mechanism would be an eosinophil-specific pathway of adhesion to vascular endothelium. In this study we have demonstrated that human eosinophils, but not neutrophils, constitutively express alpha-4-beta-1 (CD49d/CD29). Expression was not increased on low density eosinophils or normal density cells stimulated with platelet-activating factor. Eosinophils, but not neutrophils, specifically adhered to COS cells transfected with vascular adhesion molecule-1 in a alpha-4-beta-1-dependent manner. Eosinophil, but not neutrophil, adhesion to IL-1 stimulated human umbilical vascular endothelial cells was significantly inhibited by alpha-4-beta-1 mAb at both 5 h (p < 0.05) and 20 h (p < 0.001). Inhibition of both resting and platelet-activating factor- (10(-7) M) stimulated eosinophil adhesion was observed. We conclude that the alpha-4-beta-1/vascular adhesion molecule-1 adhesion pathway may be involved in specific eosinophil, as opposed to neutrophil, migration into sites of eosinophilic inflammation.

Original languageEnglish
Pages (from-to)3419-3423
Number of pages5
JournalThe Journal of Immunology
Issue number10
Publication statusPublished - 15 May 1991


  • platelet-activating-factor
  • leukocyte adhesion deficiency
  • schistosoma-mansoni
  • beta-subunit
  • integrin
  • LFA-1
  • glycoproteins
  • fibronectin
  • molecule-1
  • receptors

Cite this