Neutrophil elastase induces MUC5AC gene expression in airway epithelium via a pathway involving reactive oxygen species

American Journal of Respiratory Cell and Molecular Biology
Bernard M Fischer, Judith A Voynow

Abstract

Neutrophil-predominant airway inflammation and mucus obstruction of the airways are major pathologic features of chronic airway diseases, including cystic fibrosis and chronic bronchitis. Neutrophils release elastase, a serine protease that impairs mucociliary clearance and stimulates goblet cell metaplasia and mucin production. We previously reported that neutrophil elastase increases expression of a major respiratory mucin gene, MUC5AC, by enhancing mRNA stability. However, the molecular mechanisms of elastase-regulated MUC5AC expression are not known. We hypothesized that reactive oxygen species, generated by elastase treatment, mediate MUC5AC gene expression. To test this hypothesis, A549, a respiratory epithelial cell line, was treated with elastase in the presence or absence of the oxygen radical scavenger, dimethylthiourea, or the iron chelator, desferrioxamine. MUC5AC mRNA levels were assessed by Northern analysis. Both antioxidants significantly inhibited elastase-induced MUC5AC gene expression. Dimethylthiourea also inhibited the neutrophil elastase (NE)-induced increase in MUC5AC expression in normal human bronchial epithelial cells. To determine whether elastase treatment generated reactive oxygen species, A549 and ...Continue Reading

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