Interaction of viral infections with muscarinic receptors

Research output: Contribution to journalArticle

28 Scopus citations

Abstract

Both in humans and in experimental animals, much of the airway hyperresponsiveness that accompanies vital infections is the result of increased reflex bronchoconstriction. The M3 muscarinic receptors on the airway smooth muscle function normally during vital infections so that the direct effects of acetylcholine on the smooth muscle are not altered. In contrast, the M2 muscarinic receptors on the vagal nerve endings, which normally inhibit acetycholine release, are markedly dysfunctional during viral infections. This leads to substantial increases in acetylcholine release and potentiated reflex bronchoconstriction. Multiple mechanisms account for virus-induced M2 receptor dysfunction. Vital neuraminidase may deglycosylate the M2 receptor, decreasing acetylcholine affinity. Furthermore, both viruses and interferon-γ decrease M2 receptor gene expression. Finally, in atopic hosts, vital infection causes M2 receptor dysfunction by activating eosinophils, causing them to release major basic protein which binds to the M2 receptor, functioning as an endogenous antagonist.

Original languageEnglish (US)
Pages (from-to)59-64
Number of pages6
JournalClinical and Experimental Allergy, Supplement
Volume29
Issue number2
StatePublished - Jul 17 1999

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Keywords

  • Airway hyperresponsiveness
  • Muscarinic receptors
  • Reflex bronchoconstriction
  • Vital infection

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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