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Am J Physiol Lung Cell Mol Physiol 280: L79-L87, 2001;
1040-0605/01 $5.00
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Vol. 280, Issue 1, L79-L87, January 2001

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

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

First Department of Internal Medicine, Tohoku University School of Medicine, Sendai 980-8574, Japan

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.

neutrophil elastase; muscarinic agonist


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