Inflammatory cytokines can enhance CD44-mediated airway epithelial cell adhesion independently of CD44 expression

Shih Hsing Leir, Stephen T. Holgate, Peter M. Lackie*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

21 Scopus citations


In airways, the cell surface molecule CD44 is upregulated on bronchial epithelial cells in areas of damage. We have shown that a blocking standard CD44 (CD44s) antibody caused a 77% (± 19%) inhibition of cell migration at 3 h after mechanical damage and decreased epithelial cell repair of cells grown on cell culture filter inserts. With the use of primary human bronchial epithelial cells and the bronchial epithelial cell line 16HBE 14o-, a CD44s antibody inhibited >95% (P < 0.01) of cell binding to hyaluronic acid (HA). The cytokines TNF-α, IFN-γ, IL-1β, and IL-4 stimulated a 2- to 3.5-fold increase in CD44-dependent cell binding to HA. IFN-γ treatment did not increase CD44 expression as assessed by flow cytometry, although phorbol myristate acetate treatment did. This indicates that IFN-γ-induced cell binding to HA did not require increased CD44 expression. These data indicate that CD44 is important for bronchial epithelial cell binding to HA and that cytokines known to be expressed in inflammation can increase HA binding independently of the level of CD44 expression.

Original languageEnglish (US)
Pages (from-to)L1305-L1311
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number6 29-6
StatePublished - Dec 2003


  • Bronchial epithelium
  • Hyaluronic acid
  • IFN-γ
  • Repair
  • Wound healing

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

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