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Related Experiment Videos

Nasal mucosal endorgan hyperresponsiveness

C Svensson1, M Andersson, L Greiff

  • 1Department of Otorhinolaryngology, Head & Neck Surgery, University Hospital, Lund, Sweden.

American Journal of Rhinology
|March 26, 1998
PubMed
Summary
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Airway hyperresponsiveness in inflammatory diseases is not due to epithelial damage. Instead, mucosal exudation and glandular hyperresponsiveness are key inflammatory responses in allergic rhinitis and the common cold.

Area of Science:

  • Immunology
  • Respiratory Medicine
  • Pathophysiology

Background:

  • Nonspecific airway hyperresponsiveness is a hallmark of inflammatory airway diseases, but its mechanisms remain unclear.
  • The nose offers an accessible model for in vivo human studies of airway mucosal processes.

Purpose of the Study:

  • To investigate the role of different airway endorgans in the pathophysiology of allergic airway disease.
  • To elucidate the mechanisms underlying airway hyperresponsiveness.

Main Methods:

  • Topical challenges with methacholine, capsaicin, and histamine to assess glandular secretion, sensory nerve activation, and microvascular exudation, respectively.
  • Utilized a "nasal pool" device for concomitant provocation and lavage to measure plasma protein levels in nasal lavage fluids.

Related Experiment Videos

  • Assessed nasal absorption permeability using 51CR-EDTA and dDAVP.

    • Main Results:

    • Topical histamine challenge induced plasma exudation without altering epithelial barrier function.
    • Secretory hyperresponsiveness was observed in allergic rhinitis, developing rapidly after allergen challenge and responsive to steroids and antihistamines.
    • Exudative hyperresponsiveness was present in both allergic rhinitis and the common cold.
    • Nasal absorption permeability was decreased or unchanged in allergic and virus-induced rhinitis, refuting epithelial damage as a cause of hyperresponsiveness.

    Conclusions:

    • Mucosal exudation of plasma is a physiological defense response and a significant inflammatory mechanism in airway diseases.
    • Airway hyperresponsiveness is not explained by increased mucosal absorption due to epithelial damage.
    • The airway mucosal barrier may become functionally tighter in chronic eosinophilic inflammation.