Secretion and gene expression of secretory leukocyte protease inhibitor by human airway submucosal glands

Hiroki Saitoh, Tohru Masuda, Sanae Shimura, Toshiaki Fushimi, Kunio Shirato

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35 Citations (Scopus)


Submucosal glands were isolated within 4 h of death from tracheae and bronchi obtained from autopsied lungs, and the secretory response of secretory leukocyte protease inhibitor (SLPI) was examined with ELISA and a secretory index. Although human neutrophil elastase (HNE) at low concentrations increased SLPI secretion above the control level (i.e., 149% of control level at 10-11 M), HNE at high concentrations significantly decreased it below the control level (i.e., 16% of control level at 10-7 M). The decrease in SLPI concentration was shown to result from the degradation of SLPI by excessive HNE. Methacholine induced significant secretion (i.e., 363% of control level at 10-5 M) that was abolished by both M1 and M3 receptor antagonists. A semiquantitative analysis of SLPI mRNA by RT-PCR and Southern blot showed that compared with the superficial epithelium, submucosal glands had a 30-fold or higher level of SLPI mRNA. Both HNE and methacholine significantly increased the level of SLPI mRNA in submucosal glands in a dose-dependent manner (i.e., 357% of control level at 10-7 M and 175% of control level at 10-5 M, respectively). These findings indicate that human airway submucosal glands can transcribe 30-fold or more SLPI mRNA than the superficial epithelium and that SLPI mRNA transcription and secretion are regulated by both HNE and muscarinic receptors.

Original languageEnglish
Pages (from-to)L79-L87
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number1 24-1
Publication statusPublished - 2001 Jan


  • Muscarinic agonist
  • Neutrophil elastase

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology


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