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Articles in PresS, published online ahead of print April 12, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00455.2001
Submitted on November 26, 2001
Accepted on April 10, 2002
* To whom correspondence should be addressed. E-mail: janadel{at}itsa.ucsf.edu.
Neutrophil products are implicated in hypersecretory airway diseases. To determine the mechanisms linking a proteolytic effect of human neutrophil elastase (HNE) and mucin overproduction, we examined the effects of HNE on MUC5AC mucin production in human airway epithelial (NCI-H292) cells. Stimulation with HNE for 5 - 30 min induced MUC5AC production 24 h later, which was prevented by HNE serine active site inhibitors, implicating a proteolytic effect of HNE. MUC5AC induction was preceded by epidermal growth factor receptor (EGFR) tyrosine phosphorylation and was prevented by selective EGFR tyrosine kinase inhibitors, implicating EGFR activation. HNE-induced MUC5AC production was inhibited by a neutralizing transforming growth factor alpha (TGF-
, an EGFR ligand) antibody and by a neutralizing EGFR antibody but not by oxygen free radical scavengers, further implicating TGF- and ligand-dependent EGFR activation in the response. HNE decreased proTGF- in NCI-H292 cells and increased TGF- in cell culture supernatant. From these results, we conclude that HNE-induced MUC5AC mucin production occurs via its proteolytic activation of an EGFR signaling cascade involving TGF-.
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