Muscarinic receptor dysfunction in asthma

Allison Fryer, Richard W. Costello, David Jacoby

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Increased release of acetylcholine from the parasympathetic nerves may contribute to the hyperresponsiveness characteristic of asthma. Feedback of acetylcholine onto inhibitory M2 muscarinic receptors on the parasympathetic nerves decreases the further release of acetylcholine. Dysfunctions of these neuronal M2 receptors increases the release of acetylcholine and leads to hyperresponsiveness in animals. In antigen-challenged guinea pigs, hyperresponsiveness is entirely mediated by loss of M2 muscarinic receptor function. Loss of M2 receptor function is also associated with hyperresponsiveness in humans with asthma when they are exposed to ozone or have a naturally acquired viral infection. There are several different mechanisms for loss of M2 muscarinic receptor function, including blockade of the receptor by eosinophil major basic protein, decreased affinity of the receptor for agonists, and decreased M2-receptor gene expression. The different mechanisms are described and discussed in the context of asthma and of the various animal models of hyperresponsiveness.

Original languageEnglish (US)
Pages (from-to)63-67
Number of pages5
JournalAllergy and Clinical Immunology International
Volume12
Issue number2
StatePublished - 2000
Externally publishedYes

Fingerprint

Muscarinic Receptors
Muscarinic M2 Receptors
Acetylcholine
Asthma
Eosinophil Major Basic Protein
Ozone
Virus Diseases
Guinea Pigs
Animal Models
Gene Expression
Antigens

ASJC Scopus subject areas

  • Immunology and Allergy

Cite this

Muscarinic receptor dysfunction in asthma. / Fryer, Allison; Costello, Richard W.; Jacoby, David.

In: Allergy and Clinical Immunology International, Vol. 12, No. 2, 2000, p. 63-67.

Research output: Contribution to journalArticle

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