Inflammatory cytokines can enhance CD44-mediated airway epithelial cell adhesion independently of CD44 expression
Inflammatory cytokines can enhance CD44-mediated airway epithelial cell adhesion independently of CD44 expression
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-?, IFN-?, IL-1?, and IL-4 stimulated a 2- to 3.5-fold increase in CD44-dependent cell binding to HA. IFN-? treatment did not increase CD44 expression as assessed by flow cytometry, although phorbol myristate acetate treatment did. This indicates that IFN-?-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.
hyaluronic acid, ifn-? wound healing, repair, bronchial epithelium
L1305-L1311
Leir, Shih-Hsing
c534558c-19b3-409c-afcc-fedc66e1e3e5
Holgate, Stephen T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc
Lackie, Peter M.
4afbbe1a-22a6-4ceb-8cad-f3696dc43a7a
2003
Leir, Shih-Hsing
c534558c-19b3-409c-afcc-fedc66e1e3e5
Holgate, Stephen T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc
Lackie, Peter M.
4afbbe1a-22a6-4ceb-8cad-f3696dc43a7a
Leir, Shih-Hsing, Holgate, Stephen T. and Lackie, Peter M.
(2003)
Inflammatory cytokines can enhance CD44-mediated airway epithelial cell adhesion independently of CD44 expression.
American Journal of Physiology: Lung Cellular and Molecular Physiology, 285 (6), .
Abstract
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-?, IFN-?, IL-1?, and IL-4 stimulated a 2- to 3.5-fold increase in CD44-dependent cell binding to HA. IFN-? treatment did not increase CD44 expression as assessed by flow cytometry, although phorbol myristate acetate treatment did. This indicates that IFN-?-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.
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Published date: 2003
Keywords:
hyaluronic acid, ifn-? wound healing, repair, bronchial epithelium
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Local EPrints ID: 27225
URI: http://eprints.soton.ac.uk/id/eprint/27225
ISSN: 1040-0605
PURE UUID: 0cdb39ea-946f-480d-aac4-f7b81b442d49
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Date deposited: 27 Apr 2006
Last modified: 16 Mar 2024 02:45
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Author:
Shih-Hsing Leir
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