Noninflammatory Mechanisms in Virus-Induced Wheezing
Additional noninflammatory mechanisms may contribute to the development of wheezing following viral RTI. Viral infection of respiratory epithelium results in reduced nitric oxide production associated with AHR in guinea pigs. Nitric oxide is the putative bronchodilator agonist of the nonadrenergic, noncholinergic inhibitory (NANCi) system. This system can be defective during and after respiratory viral infection resulting in AHR, as demonstrated in a study of RSV infection of cotton rats.
A reduced barrier function of the respiratory epithelium may expose sensory C fibers to enhanced stimulation. This results in the release of neuropeptides, such as substance P and neurokinin A, both agonists of the nonadrenergic, noncholinergic activating system; further, it induces a brainstem reflex leading to bronchoconstriction. Neuropeptides can also contribute to airway obstruction by causing increased leukotriene synthesis, release of mast cell mediators, and increased mucus secretion. In addition, infected epithelial cells produce smaller amounts of neutral endopeptidase, an enzyme that degrades neuropeptides. The role of sensory C fibers in virus-induced asthma exacerbations in humans remains controversial. Bradykinin provocation following experimental rhinovirus infection in mild asthmatics does not result in increased bronchial hyperresponsiveness. Bradykinin is a strong stimulator of sensory C fibers and may be expected to cause increased bronchial hyperresponsiveness if this system plays a major part in virus-induced asthma.
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Cite this: Respiratory Viral Infections and Asthma: Is There a Link? - Medscape - Jul 13, 2000.