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Cardiovascular Research Institute and Departments of Medicine and Physiology, University of California, San Francisco, CA 94143
Eosinophil recruitment and mucus hypersecretion are characteristic
of asthmatic airway inflammation, but eosinophils have not been shown
to induce mucin production. Because an epidermal growth factor receptor
(EGFR) cascade induces MUC5AC mucin in airways, and because EGFR is
up-regulated in asthmatic airways, we examined the effect of
eosinophils on MUC5AC mucin production in NCI-H292 cells (a human
airway epithelial cell line that produces mucins). Eosinophils were
isolated from the peripheral blood of allergic patients, and their
effects on MUC5AC mucin gene and protein synthesis
were assessed using in situ hybridization and ELISAs. When IL-3 plus
GM-CSF or IL-3 plus IL-5 were added to eosinophils cultured with
NCI-H292 cells, MUC5AC mucin production increased; eosinophils or
cytokines alone had no effect. Eosinophil supernatant obtained by
culturing eosinophils with IL-3 plus GM-CSF or IL-3 plus IL-5 also
increased MUC5AC synthesis in NCI-H292 cells, an effect that was
prevented by selective EGFR inhibitors (AG1478, BIBX1522). Supernatant
of activated eosinophils induced EGFR phosphorylation in NCI-H292
cells. Supernatant of activated eosinophils contained increased
concentrations of TGF-
protein (an EGFR ligand) and induced
up-regulation of TGF- expression and release in NCI-H292 cells. A
blocking Ab to TGF- reduced activated eosinophil-induced MUC5AC
synthesis in NCI-H292 cells. These results show that activated
eosinophils induce mucin synthesis in human airway epithelial cells via
EGFR activation, and they implicate TGF- produced by eosinophils and
epithelial cells in the EGFR activation that results in mucin
production in human airway epithelium.
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