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Immunoreactive interleukin-1 (IL-1) α and β levels in nasal polyp (NP) extracts were measured from 22 adult patients with chronic sinusitis (CS) in order to determine their significance in the pathogenesis of NP. The NP sample was separated into mononuclear and polymorphonuclear fractions. In the mononuclear fraction, the mean value of IL-1β was 21.5 pg/ml/g, which was significantly higher than that of IL-1α (8.4pg/ml/g, p < 0.01). In younger adults, the IL-1α and IL-1β levels were 21.2 and 59.4 pg/ml/g, which were significantly higher than those in older CS patients (p < 0.01). There was a significant reverse correlation between patient’s age and IL-1β levels in the mononuclear fraction (r=––0.509, p < 0.01). Immunoreactive IL-1, mainly IL-1β, was identified in the cytoplasmic area of monocytes. A certain amount of immunoreactive IL-1 is produced in mononuclear leukocytes, particularly activated monocytes, and IL-1β production is greater than IL-1α. In younger adult CS patients, NPs contain larger amounts of IL-1β in monocytes, compared to those of older patients.

Vasoactive intestinal peptide (VIP) and nitric oxide (NO) are neurotransmitters involved in the regulation of bronchial and pulmonary vascular tone. Published studies of the effects of VIP on airway mucus secretion have yielded conflicting results. The purpose of this study was to determine the effect of VIP on mucus secretion in the ferret trachea and if this effect was influenced by NO. We used a sandwich enzyme-linked lectin assay to measure mucin secretion and a turbidimetric assay to measure lysozyme (serous cell) secretion from ferret tracheal segments. VIP (10(-7) M) increased mucin secretion over 2 h. VIP (10(-9) to 10(-5) M) stimulated mucin secretion in a dose-dependent fashion. VIP-induced mucin secretion was partially blocked by a VIP receptor antagonist (a chimeric VIP-pituitary adenylate cyclase-activating peptide analog, VIP receptor antagonist) at a 10-fold excess concentration. At all concentrations tested, neither NG-nitro-L-arginine methyl ester, an inhibitor of NO synthase, nor S-nitroso-N-acetyl-penicillamine, an NO donor, had any significant effect on constitutive or VIP-induced mucus secretion. We conclude that VIP-stimulated mucin and lysozyme secretion was both time dependent and dose dependent and that NO neither stimulates nor inhibits mucus secretion in the ferret trachea.

Our results indicate that RHNM may be useful for studying the topical effects of various drugs on nasal mucus from patients with chronic sinusitis.

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