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Am J Physiol Lung Cell Mol Physiol (April 25, 2003). doi:10.1152/ajplung.00046.2003
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Submitted on February 14, 2003
Accepted on April 17, 2003

Dexamethasone prevents virus induced hyperresponsiveness via multiple mechanisms

Liliana Moreno1, David B. Jacoby2, and Allison D. Fryer1*

1 Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA
2 Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA

* To whom correspondence should be addressed. E-mail: afryer{at}jhsph.edu.

In the lungs, neuronal M2 muscarinic receptors inhibit acetylcholine release from the parasympathetic nerves. Parainfluenza virus infection causes loss of M2 receptor function, which increases acetylcholine release and vagally mediated bronchoconstriction. Since glucocorticoids are known to inhibit airway hyperresponsiveness, we tested whether dexamethasone (6.5 µg/kg or 65 µg/kg, i.p.) prevents virus-induced hyperresponsiveness and M2 receptor dysfunction in guinea pigs. In controls, pilocarpine, a muscarinic agonist, inhibited vagally induced bronchoconstriction, demonstrating functional M2 receptors. However, in virus-infected animals, pilocarpine failed to inhibit vagally induced bronchoconstriction demonstrating M2 receptor dysfunction. Frequency dependent bronchoconstriction was greater in virus infected than in controls, indicating airway hyperresponsiveness. Low dose dexamethasone (6.5 µg/kg i.p.) treatment prevented virus induced airway hyperresponsiveness, ameliorated M2R dysfunction, and decreased viral content in the lungs without inhibiting virus induced inflammation. High dose dexamethasone (65 µg/kg i.p.) prevented virus induced hyperresponsiveness, completely reversed M2 receptor dysfunction, decreased viral titers, and decreased virus induced inflammation. This high dose dexamethasone also increased M2 receptor function in uninfected animals. In conclusion, dexamethasone prevented virus induced hyperresponsiveness and M2 receptor dysfunction via multiple mechanisms.




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