Pathophysiology of airway viral infections

Research output: Contribution to journalArticle

21 Scopus citations

Abstract

Viral infections are major causes of cough. Virus-induced changes in airway sensory nerve function include increased tachykinin expression and, more specifically, expression of tachykinins by Aδ fibers. This change may be mediated by neurotrophins produced in response to viral infection. At the same time, activity of neutral endopeptidase, an enzyme that is important in degrading and inactivating tachykinins, is decreased by airway viral infections. Viral infections can activate eosinophils, releasing proteins that can cause tachykinin release. Moreover, expression of the NK1 receptor is increased by viral infections of the lungs. The expression of M2 muscarinic receptors, which normally decrease the sensitivity of sensory nerves, is decreased by viral infections. So it is possible that viral infections (1) increase expression of tachykinins (by causing neurotrophin expression), (2) increase release of tachykinins (by causing release of eosinophil proteins), (3) decrease degradation of tachykinins (by decreasing neutral endopeptidase activity), (4) increase expression of the NK1 receptor (again mediated by neurotrophins), and (5) increase the sensitivity of airway afferents (by decreasing M2 muscarinic receptor expression). All these changes may potentiate the tachykininergic input into the cough reflex, and may provide new therapeutic targets for controlling virus-induced cough.

Original languageEnglish (US)
Pages (from-to)333-336
Number of pages4
JournalPulmonary Pharmacology and Therapeutics
Volume17
Issue number6 SPEC.ISS.
DOIs
StatePublished - Dec 2004

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Keywords

  • Airway epithelium
  • Eosinophils
  • Interferons
  • Muscarinic receptors
  • Tachykinins
  • Viral infections

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Biochemistry, medical
  • Pharmacology (medical)

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