Toxic rhinitis-induced changes of human nasal mucosa innervation

Irritative toxic rhinitis is a nasal disorder induced by chemical compounds like ozone, formaldehyde, nickel, chrome, solvents and tobacco smoke. These noxious stimuli may have effects on the nasal innervation leading to a cascade of neuro-immune interactions and an augmentation of the symptoms. Her...

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Bibliographic Details
Published in:Toxicologic pathology 2003-05, Vol.31 (3), p.326-331
Main Authors: GRONEBERG, David A, HEPPT, Werner, CRYER, Annette, WUSSOW, Anke, PEISER, Christian, ZWENG, Martina, THAI DINH, Q, WITT, Christian, FISCHER, Axel
Format: Article
Language:English
Subjects:
Adolescent
Adult
Aged
Biological and medical sciences
Calcitonin Gene-Related Peptide - metabolism
Eosinophils - pathology
Female
Humans
Male
Mast Cells - pathology
Medical sciences
Middle Aged
Nasal Mucosa - innervation
Nasal Mucosa - metabolism
Nasal Mucosa - pathology
Nerve Fibers - metabolism
Nerve Fibers - pathology
neuropeptides
Neuropeptides - metabolism
Non tumoral diseases
Otorhinolaryngology. Stomatology
Rhinitis - etiology
Rhinitis - metabolism
Rhinitis - pathology
Substance P - metabolism
Tobacco Smoke Pollution - adverse effects
toxic rhinitis
Upper respiratory tract, upper alimentary tract, paranasal sinuses, salivary glands: diseases, semeiology
Vasoactive Intestinal Peptide - metabolism
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Summary:Irritative toxic rhinitis is a nasal disorder induced by chemical compounds like ozone, formaldehyde, nickel, chrome, solvents and tobacco smoke. These noxious stimuli may have effects on the nasal innervation leading to a cascade of neuro-immune interactions and an augmentation of the symptoms. Here we examined changes in the neuropeptide content of mucosal parasympathetic, sympathetic and sensory nerves of patients with toxic rhinitis caused by chronic cigarette smoke exposure. Semiquantitative immunohistochemistry using antibodies against calcitonin gene-related peptide (CGRP), substance P (SP), neuropeptide tyrosine (NPY), and vasoactive intestinal peptide (VIP) was carried out on cryostat sections of human nasal mucosa obtained from normal subjects and patients with toxic rhinitis and revealed significant differences between both groups. Toxic rhinitis patients had significantly elevated expression scores for VIP (2.83 +/- 0.31 vs 1.27 +/- 0.47 control group) and NPY (3.17 +/- 0.31 vs 0.91 +/- 0.37 control group) revealing an increase of mediators in distinct subpopulations of airway nerves. In summary, the present studies indicate a differential participation of subclasses of mucosal nerves in the pathophysiology of toxic rhinitis. Airway innervation may have a major role in the pathophysiology of toxic rhinitis associated with chronic cigarette smoke exposure.
ISSN:0192-6233
1533-1601
DOI:10.1080/01926230309749