Neuropathology in Rhinosinusitis

Am. J. Respir. Crit. Care Med. published 11 October 2004,

http://ajrccm.atsjournals.org/cgi/content/abstract/200403-357OCv1?ct

Published ahead of print on October 11, 2004
Submitted on June 9, 2004
Accepted on October 4, 2004

James N Baraniuk1*, Kristina Naranch Petrie1, Uyenphuong Le1, Chih -
Feng Tai2, Yong - Jin Park3, Atsushi Yuta4, Mushtaq Ali1, Christopher J
VandenBussche1, and Benjamin Nelson1

1 Division of Rheumatology, Immunology and Allergy, Georgetown
University, Washington, DC, United States, 2 Department of
Otorhinolaryngology, Kaohsiung Medical University, Kaohsiung City,
Taiwan, 3 Department of Otorhinolaryngology, Catholic University, Seoul,
Korea, 4 Department of Otorhinolaryngology, Mie University, Tsu, Japan

* E-mail: baraniuj@georgetown.edu.

Pathophysiological differences in neural responses to hypertonic saline
were investigated in acute sinusitis (n=25), chronic fatigue syndrome
subjects with nonallergic rhinitis (n=14), active allergic rhinitis
(n=17) and normal (n=20) subjects. 

Increasing strengths of hypertonic
saline were sprayed into their nostrils at 5 min 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 allergic rhinitis 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. Chronic fatigue syndrome had neural hypersensitivity
(pain) but reduced serous cell secretion. Hypertonic saline nasal
provocations identified significant, unique patterns of neural and
mucosal dysregulation in each rhinosinusitis syndrome.


Key words: Neurogenic inflammation, axon response, mucosal
hyperresponsiveness, glandular exocytosis, urea secretion