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Background: Excessive mucus secretion is an important characteristic of airway inflammatory diseases, such as asthma. Lipopolysaccharide (LPS) leads to mucus hypersecretion in asthma, and is associated with airway inflammation and remodeling. It is known little about the role of epidermal growth factor receptor (EGFR) in LPS-induced mucin 5AC (MUC5AC) hypersecretion in human bronchial epithelial cells. We aim to investigate the effects of EGFR in the process of MUC5AC hypersecretion. Methods: The human bronchial epithelial (16HBE) cells were treated with LPS, and pre-treated with AG1478 (specific inhibitor of EGFR). The expression of MUC5AC and EGFR were detected and compared between the different groups. The expression of MUC5AC protein was measured by enzyme linked immunosorbent assay (ELISA). The expressions of MUC5AC and EGFR were measured by immunohistochemistry, and the protein expression of EGFR was monitored by Western blot. The mRNA expression of MUC5AC and EGFR were detected by reverse transcription-polymerase chain reaction (RT-PCR). Results and Conclusions: LPS could induce the high expression of MUC5AC and EGFR in 16HBE cells, and AG1478 decreased the expression of MUC5AC by inhibiting the expression of EGFR. These results showed that EGFR might play an important role in LPS-induced MUC5AC hypersecretion of airway epithelial cells, and AG1478 decreased MUC5AC secretion through inhibiting the expression of EGFR. AG1478 may be a new therapeutic approach for the airway inflammatory diseases.

EGFR plays an essential role in lipopolysaccharide (LPS)-induced MUC5AC hypersecretion in human bronchial epithelial cells