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Am J Physiol Lung Cell Mol Physiol (August 8, 2003). doi:10.1152/ajplung.00255.2002
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Submitted on August 2, 2002
Accepted on August 7, 2003

Inflammatory cytokines can enhance CD44-mediated airwayepithelial cell adhesion independent of CD44 expression

Shih-Hsing Leir1, Stephen T. Holgate1, and Peter M. Lackie1*

1 Respiratory Cell & Molecular Biology, Infection Immunity and Repair Division, Southampton General Hospital, Southampton, Hampshire, United Kingdom

* To whom correspondence should be addressed. E-mail: p.m.lackie{at}soton.ac.uk.

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




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