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Articles in PresS, published online ahead of print February 22, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00404.2001
Submitted on October 17, 2001
Accepted on February 14, 2002
1 Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, USA
* To whom correspondence should be addressed. E-mail: janadel{at}itsa.ucsf.edu.
Previous work showed that the Th2 cytokine, interleukin (IL)-13, induces goblet cell metaplasia via an indirect mechanism involving the expression and subsequent activation of epidermal growth factor receptor (EGFR). Because clara cell secretory protein (CCSP) expression has been reported in cells that express mucins, we examined the effect of IL-13 on CCSP gene and protein expression in pathogen-free rat airways and in pulmonary mucoepidermoid NCI-H292 cells. Intratracheal instillation of IL-13 induced CCSP mRNA in epithelial cells without cilia within 8 to 16 h, maximal between 24 and 48 h; CCSP immunostaining increased in a time-dependent fashion, maximal at 48 h. The CCSP immunostaining was localized in nongranulated secretory cells, goblet cells, and in the lumen. Pretreatment with the selective EGFR tyrosine kinase inhibitor, BIBX1522, cyclophosphamide (an inhibitor of bone marrow leukocyte mobilization), or with a blocking antibody to IL-8, prevented CCSP staining. Treatment of NCI-H292 cells with the EGFR ligand, transforming growth factor (TGF)-
, but not with IL-13 alone, induced CCSP gene and protein expression. Selective EGFR tyrosine kinase inhibitors, BIBX1522 and AG1478, prevented CCSP expression in NCI-H292 cells, but the platelet-derived growth factor receptor (PDGFR) tyrosine kinase inhibitor, AG1295, had no effect. These findings indicate that IL-13 induces CCSP expression via an EGFR- and leukocyte-dependent pathway.
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