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Am J Physiol Lung Cell Mol Physiol 276: L709-L714, 1999;
1040-0605/99 $5.00
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Vol. 276, Issue 5, L709-L714, May 1999

Antigen-induced hyperreactivity to histamine: role of the vagus nerves and eosinophils

Richard W. Costello1, Christopher M. Evans1, Bethany L. Yost1, Kristen E. Belmonte1, Gerald J. Gleich2, David B. Jacoby1,3, and Allison D. Fryer1

1 Department of Environmental Health Sciences, School of Hygiene and Public Health, and 3 Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21205; and 2 Departments of Immunology and Medicine, Mayo Clinic, Rochester, Minnesota 55905

M2 muscarinic receptors limit acetylcholine release from the pulmonary parasympathetic nerves. M2 receptors are dysfunctional in antigen-challenged guinea pigs, causing increased vagally mediated bronchoconstriction. Dysfunction of these M2 receptors is due to eosinophil major basic protein, which is an antagonist for M2 receptors. Histamine-induced bronchoconstriction is composed of a vagal reflex in addition to its direct effect on airway smooth muscle. Because hyperreactivity to histamine is seen in antigen-challenged animals, we hypothesized that hyperreactivity to histamine may be due to increased vagally mediated bronchoconstriction caused by dysfunction of M2 receptors. In anesthetized, antigen-challenged guinea pigs, histamine-induced bronchoconstriction was greater than that in control guinea pigs. After vagotomy or atropine treatment, the response to histamine in antigen-challenged animals was the same as that in control animals. In antigen-challenged animals, blockade of eosinophil influx into the airways or neutralization of eosinophil major basic protein prevented the development of hyperreactivity to histamine. Thus hyperreactivity to histamine in antigen-challenged guinea pigs is vagally mediated and dependent on eosinophil major basic protein.

muscarinic receptors; parasympathetic nerves; inflammation; major basic protein; adhesion molecules


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