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J Appl Physiol 87: 1272-1278, 1999;
8750-7587/99 $5.00
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Vol. 87, Issue 4, 1272-1278, October 1999

INVITED REVIEW
Ozone-induced hyperresponsiveness and blockade of M2 muscarinic receptors by eosinophil major basic protein

Bethany L. Yost1, Gerald J. Gleich2, and Allison D. Fryer1

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

Control of airway smooth muscle is provided by parasympathetic nerves that release acetylcholine onto M3 muscarinic receptors. Acetylcholine release is limited by inhibitory M2 muscarinic receptors. In antigen-challenged guinea pigs, hyperresponsiveness is due to blockade of neuronal M2 receptors by eosinophil major basic protein (MBP). Because exposure of guinea pigs to ozone also causes M2 dysfunction and airway hyperresponsiveness, the role of eosinophils in ozone-induced hyperresponsiveness was tested. Animals were exposed to filtered air or to 2 parts/million ozone for 4 h. Twenty-four hours later, the muscarinic agonist pilocarpine no longer inhibited vagally induced bronchoconstriction in ozone-exposed animals, indicating M2 dysfunction. M2 receptor function in ozone-exposed animals was protected by depletion of eosinophils with antibody to interleukin-5 and by pretreatment with antibody to guinea pig MBP. M2 function was acutely restored by removal of MBP with heparin. Ozone-induced hyperreactivity was also prevented by antibody to MBP and was reversed by heparin. These data show that loss of neuronal M2 receptor function after ozone is due to release of eosinophil MBP.

neuronal receptors; hyperreactivity; asthma; inflammation


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