Interaction of viral infections with muscarinic receptors

Research output: Contribution to journalArticle

28 Citations (Scopus)

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 - 1999
Externally publishedYes

Fingerprint

Muscarinic Receptors
Virus Diseases
Bronchoconstriction
Acetylcholine
Smooth Muscle
Reflex
Infection
Muscarinic M3 Receptors
Muscarinic M2 Receptors
Viruses
Nerve Endings
Neuraminidase
Cholinergic Receptors
Eosinophils
Interferons
Gene Expression
Proteins

Keywords

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

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Interaction of viral infections with muscarinic receptors. / Jacoby, David; Fryer, Allison.

In: Clinical and Experimental Allergy, Supplement, Vol. 29, No. 2, 1999, p. 59-64.

Research output: Contribution to journalArticle

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