The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1999/11/1465/ $5.00
The Journal of Experimental Medicine, Volume 190, Number 10, November 15, 1999 1465-1478

Original Article

Ovalbumin Sensitization Changes the Inflammatory Response to Subsequent Parainfluenza Infection: Eosinophils Mediate Airway Hyperresponsiveness, M2 Muscarinic Receptor Dysfunction, and Antiviral Effects

Darryl J. Adamkob, Bethany L. Yosta, Gerald J. Gleichd, Allison D. Fryera, and David B. Jacobya,c
a Department of Environmental Health Sciences, School of Hygiene and Public Health,
b Department of Pediatrics, School of Medicine, Johns Hopkins University, Baltimore, Maryland 21205
c Department of Internal Medicine, School of Medicine, Johns Hopkins University, Baltimore, Maryland 21205
d Department of Immunology and the Department of Medicine, Mayo Clinic, Rochester, Minnesota 55905

Correspondence to: David B. Jacoby, Division of Pulmonary and Critical Care Medicine, School of Medicine, Johns Hopkins University, 5501 Hopkins Bayview Circle, Baltimore, MD 21224. Tel:410-550-0545 Fax:410-955-0299 E-mail:djacoby{at}welchlink.welch.jhu.

Asthma exacerbations, many of which are virus induced, are associated with airway eosinophilia. This may reflect altered inflammatory response to viruses in atopic individuals. Inhibitory M2 muscarinic receptors (M2Rs) on the airway parasympathetic nerves limit acetylcholine release. Both viral infection and inhalational antigen challenge cause M2R dysfunction, leading to airway hyperresponsiveness. In antigen-challenged, but not virus-infected guinea pigs, M2R dysfunction is due to blockade of the receptors by the endogenous antagonist eosinophil major basic protein (MBP). We hypothesized that sensitization to a nonviral antigen before viral infection alters the inflammatory response to viral infection, so that M2R dysfunction and hyperreactivity are eosinophil mediated. Guinea pigs were sensitized to ovalbumin intraperitoneally, and 3 wk later were infected with parainfluenza. In sensitized, but not in nonsensitized animals, virus-induced hyperresponsiveness and M2R dysfunction were blocked by depletion of eosinophils with antibody to interleukin (IL)-5 or treatment with antibody to MBP. An additional and unexpected finding was that sensitization to ovalbumin caused a marked (80%) reduction in the viral content of the lungs. This was reversed by the antibody to IL-5, implicating a role for eosinophils in viral immunity.

Key Words: eosinophils, muscarinic receptors, parainfluenza virus, antigen challenge, viral immunity


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