Osteopontin is expressed and functional in human eosinophils

I. Puxeddu, N. Berkman, D. Ribatti, R. Bader, H. M. Haitchi, D. E. Davies, P. H. Howarth, F. Levi-Schaffer*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

65 Scopus citations


Background: Eosinophils are critically involved in allergic inflammation and tissue remodeling. Osteopontin (OPN) is a glycoprotein molecule which exhibits pro-fibrogenic and pro-angiogenic properties and has recently also been implicated in allergic diseases. In this study, we investigated the expression and function of OPN in human eosinophils. Methods: Osteopontin mRNA (RT-PCR) and protein (immunofluorescence) expression in peripheral blood eosinophils from atopic human subjects were evaluated. Soluble OPN release was determined in resting and activated eosinophils. The contribution of OPN to eosinophil-induced angiogenesis was determined using the chick embryo chorio- allantoic membrane (CAM) assay and OPN-induced eosinophil chemotaxis was determined (ChemoTx System microplate wells). Finally, OPN expression in bronchoalveolar lavage (BAL) fluids from mild asthmatic and normal control subjects was determined. Results: Osteopontin is expressed in human eosinophils and is increased following GM-CSF and IL-5 activation. Eosinophil-derived OPN contributes to eosinophil-induced angiogenesis. Recombinant OPN promotes eosinophil chemotaxis in vitro and this effect is mediated by α4β1 integrin binding. Soluble OPN is increased in the bronchoalveolar lavage fluid from mild asthmatic subjects and correlates with eosinophil counts. Conclusions: We therefore conclude that OPN is likely to contribute to the process of angiogenesis observed in the airways in asthma.

Original languageAmerican English
Pages (from-to)168-174
Number of pages7
JournalAllergy: European Journal of Allergy and Clinical Immunology
Issue number2
StatePublished - Feb 2010


  • Airway remodeling
  • Allergic inflammation
  • Angiogenesis
  • Eosinophils
  • Osteopontin


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