Role of neutrophil elastase in endotoxin-induced mucus hypersecretion in rat nasal epithelium

Ann Otol Rhinol Laryngol. 2000 Nov;109(11):1049-54. doi: 10.1177/000348940010901111.

Abstract

In 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.

MeSH terms

  • Animals
  • Endotoxins / metabolism*
  • Escherichia coli*
  • Goblet Cells / pathology
  • Hypertrophy / pathology
  • Leukocyte Elastase / physiology*
  • Male
  • Mucus / metabolism*
  • Nasal Mucosa / metabolism*
  • Nasal Mucosa / pathology
  • Rats
  • Rats, Inbred F344
  • Time Factors

Substances

  • Endotoxins
  • Leukocyte Elastase