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Ann Oto Rhinol Laryn · Nov 2000
Role of neutrophil elastase in endotoxin-induced mucus hypersecretion in rat nasal epithelium.
- T Shimizu, Y Takahashi, K Takeuchi, Y Majima, and Y Sakakura.
- Department of Otorhinolaryngology, Mie University School of Medicine, Tsu, Japan.
- Ann Oto Rhinol Laryn. 2000 Nov 1; 109 (11): 1049-54.
AbstractIn the present study, hypertrophic and metaplastic changes of goblet cells were induced in rat nasal epithelium by intranasal instillation of endotoxin or elastase. A significant increase in the amount of intraepithelial mucosubstance was observed after 24 hours during 3 days of instillation. The elastase-induced mucus production was not inhibited in neutrophil-depleted rats, but the endotoxin-induced change was significantly inhibited. Intranasal instillation of the neutrophil elastase inhibitor ONO-5046 partially inhibited the endotoxin-induced mucus production. Epithelial mucus secretion was evaluated by the temporary decrease in the amount of intraepithelial mucosubstance. The endotoxin-induced mucus secretion peaked 3 to 6 hours after intranasal instillation, coinciding with the peak of the intraepithelial neutrophil infiltration. The elastase-induced mucus secretion peaked 1 to 3 hours after intranasal instillation; intraepithelial neutrophil infiltration was not induced by elastase. These results indicate that neutrophil elastase is an important mediator of the intraepithelial mucus synthesis and secretion induced by endotoxin.
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