Cutting edge: Expression of the C-C chemokine receptor CCR3 in human airway epithelial cells

C. Stellato, M. E. Brummet, J. R. Plitt, S. Shahabuddin, F. M. Baroody, M. C. Liu, P. D. Ponath, L. A. Beck

Research output: Contribution to journalArticle

Abstract

Chemokine-induced eosinophil chemotaxis is mediated primarily through the C-C chemokine receptor, CCR3. We have now detected CCR3 immunoreactivity on epithelial cells in biopsies of patients with asthma and other respiratory diseases. CCR3 mRNA was detected by Northern blot analysis after TNF-α stimulation of the human primary bronchial epithelial cells as well as the epithelial cell line, BEAS-2B; IFN-γ potentiated the TNF-αinduced expression. Western blots and flow cytometry confirmed the expression of CCR3 protein. This receptor is functional based on studies demonstrating eotaxin-induced intracellular Ca2+ flux and tyrosine phosphorylation of cellular proteins. The specificity of this functional response was confirmed by blocking these signaling events with anti-CCR3 mAb (7B11) or pertussis toxin. Furthermore, 125I-eotaxin binding assay confirmed that CCR3 expressed on epithelial cells have the expected ligand specificity. These studies indicate that airway epithelial cells express CCR3 and suggest that CCR3 ligands may influence epithelial cell functions.

Original languageEnglish (US)
Pages (from-to)1457-1461
Number of pages5
JournalJournal of Immunology
Volume166
Issue number3
DOIs
StatePublished - Feb 1 2001

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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