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Cardiovascular Research Institute and Departments of Medicine and Physiology, University of California, San Francisco, California 94143-0130
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
8-16 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 and
goblet cells and in the lumen. Pretreatment with the selective EGFR
tyrosine kinase inhibitor BIBX1522, cyclophosphamide (an inhibitor of
bone marrow leukocyte mobilization), or a blocking antibody to IL-8
prevented CCSP staining. Treatment of NCI-H292 cells with the EGFR
ligand transforming growth factor-
, 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
tyrosine kinase inhibitor AG1295 had no effect. These findings
indicate that IL-13 induces CCSP expression via an EGFR- and
leukocyte-dependent pathway.
Clara cell 10-kDa protein; epidermal growth factor receptor; goblet cell; interleukin-13; secretoglobin; uteroglobin
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