Journal
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
Volume 171, Issue 1, Pages 5-11Publisher
AMER THORACIC SOC
DOI: 10.1164/rccm.200403-357OC
Keywords
axon response; glandular exocytosis; mucosal hyperresponsiveness; neurogenic inflammation; urea secretion
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Funding
- NCRR NIH HHS [1 M01-RR13297-01A1] Funding Source: Medline
- NIAID NIH HHS [R01 AI042403, R01 AI 42403] Funding Source: Medline
- NATIONAL CENTER FOR RESEARCH RESOURCES [M01RR013297] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI042403] Funding Source: NIH RePORTER
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Pathophysiologic differences in neural responses to hypertonic saline (HITS) were investigated in subjects with acute sinusitis (n = 25), subjects with chronic fatigue syndrome (CFS) with nonallergic rhinitis (n = 14), subjects with active allergic rhinitis (AR; n = 17), and normal (n = 20) subjects. Increasing strengths of HTS were sprayed into their nostrils at 5-minute intervals. Sensations of nasal pain, blockage, and drip increased with concentration and were significantly elevated above normal. These parallels suggested activation of similar subsets of afferent neurons. Urea and lysozyme secretion were dose dependent in all groups, suggesting that serous cell exocytosis was one source of urea after neural stimulation. Only AIR and normal groups had mucin dose responses and correlations between symptoms and lysozyme secretion (R-2 = 0.12-0.23). The lysozyme dose responses may represent axon responses in these groups. The neurogenic stimulus did not alter albumin (vascular) exudation in any group. Albumin and mucin concentrations were correlated in sinusitis, suggesting that nonneurogenic factors predominated in sinusitis mucous hypersecretion. CFS had neural hypersensitivity (pain) but reduced serous cell secretion. HTS nasal provocations identified significant, unique patterns of neural and mucosal dysregulation in each rhinosinusitis syndrome.
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