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Neuroimmune interactions in the airways: implications for asthma, allergy, and other inflammatory airway diseases.

Authors
  • Saria, A1
  • 1 Department of Psychiatry, University of Innsbruck Medical School, Austria. , (Austria)
Type
Published Article
Journal
Brain, behavior, and immunity
Publication Date
Dec 01, 1988
Volume
2
Issue
4
Pages
318–321
Identifiers
PMID: 3076481
Source
Medline
License
Unknown

Abstract

Recent evidence suggests that several bioactive polypeptides, among them substance P, neurokinin A, and calcitonin gene-related peptide, are contained in tracheobronchial C-fibers. These peptides can be released from the lung by irritant chemicals or local inflammatory mediators like histamine or bradykinin. Substance P mimics the increase in vascular permeability caused by vagal nerve stimulation and neurokinin A mimics noncholinergic bronchoconstriction by vagal nerve stimulation. Calcitonin gene-related peptide displays vasodilator activity. Experiments carried out with sensitized guinea pigs showed a contribution of tracheobronchial C-fibers to the anaphylactic response. Additionally, capsaicin, which in high concentration selectively blocks sensory C-fibers, was found to be effective in treatment of hyperreactive rhinopathy (vasomotor rhinitis). It is concluded that peptide mediators released from tracheobronchial C-fibers may contribute to the pathophysiology of various allergic or inflammatory airway diseases.

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