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Research Article Free access | 10.1172/JCI1114

Virus- and interferon-induced loss of inhibitory M2 muscarinic receptor function and gene expression in cultured airway parasympathetic neurons.

D B Jacoby, H Q Xiao, N H Lee, Y Chan-Li, and A D Fryer

Division of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21209, USA.

Find articles by Jacoby, D. in: JCI | PubMed | Google Scholar

Division of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21209, USA.

Find articles by Xiao, H. in: JCI | PubMed | Google Scholar

Division of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21209, USA.

Find articles by Lee, N. in: JCI | PubMed | Google Scholar

Division of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21209, USA.

Find articles by Chan-Li, Y. in: JCI | PubMed | Google Scholar

Division of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21209, USA.

Find articles by Fryer, A. in: JCI | PubMed | Google Scholar

Published July 1, 1998 - More info

Published in Volume 102, Issue 1 on July 1, 1998
J Clin Invest. 1998;102(1):242–248. https://doi.org/10.1172/JCI1114.
© 1998 The American Society for Clinical Investigation
Published July 1, 1998 - Version history
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Abstract

Viral infections increase vagally mediated reflex bronchoconstriction. Decreased function of inhibitory M2 muscarinic receptors on the parasympathetic nerve endings is likely to contribute to increased acetylcholine release. In this study, we used cultured airway parasympathetic neurons to determine the effects of parainfluenza virus and of interferon (IFN)-gamma on acetylcholine release, inhibitory M2 receptor function, and M2 receptor gene expression. In control cultures, electrically stimulated acetylcholine release increased when the inhibitory M2 receptors were blocked using atropine (10(-)5 M) and decreased when these receptors were stimulated using methacholine (10(-)5 M). Acetylcholine release was increased by viral infection and by treatment with IFN-gamma (300 U/ml). In these cells, atropine did not further potentiate, nor did methacholine inhibit, acetylcholine release, suggesting decreased inhibitory M2 receptor function and/or expression. Using a competitive reverse transcription-polymerase chain reaction method, we demonstrated that M2 receptor gene expression was decreased by more that an order of magnitude both by virus infection and by treatment with IFN. Thus, viral infections may increase vagally mediated bronchoconstriction both by directly inhibiting M2 receptor gene expression and by causing release of IFN-gamma which inhibits M2 receptor gene expression.

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