Published ahead of print on October 11, 2004, doi:10.1164/rccm.200403-357OC
© 2005 American Thoracic Society doi: 10.1164/rccm.200403-357OC
Neuropathology in RhinosinusitisDivision of Rheumatology, Immunology and Allergy, Georgetown University, Washington, DC; Department of Otorhinolaryngology, Kaohsiung Medical University, Kaohsiung City, Taiwan; Department of Otorhinolaryngology, Catholic University, Seoul, Korea; and Department of Otorhinolaryngology, Mie University, Tsu, Japan Correspondence and requests for reprints should be addressed to James N. Baraniuk, M.D., Division of Rheumatology, Immunology and Allergy, Room B107, Lower Level, Kober Cogan Building, Georgetown University, 3800 Reservoir Road, N.W., Washington, DC 20007–2197. E-mail: baraniuj{at}georgetown.edu Pathophysiologic differences in neural responses to hypertonic saline (HTS) 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 AR and normal groups had mucin dose responses and correlations between symptoms and lysozyme secretion (R2 = 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.
Key Words: axon response • glandular exocytosis • mucosal hyperresponsiveness • neurogenic inflammation • urea secretion This article has been cited by other articles:
|
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
