Many of the symptoms of allergic airway disease such as sneezing, coughing, excessive secretions, reflex bronchoconstriction, and dyspnea occur secondary to changes in the activity of the airway nervous system. In addition, many subjects with allergic airway disease have a heightened sensitivity to non-immunologic irritants in the environment. The symptoms and heightened sensitivities may be explained largely as a consequence of allergen-induced neuromodulation. Mediators associated with allergic inflammation can modulate primary afferent nerves, their connecting neurons in the central nervous system, as well as efferent autonomic neurons innervating the airways. This modulation can take the form of acute electrophysiological changes, or more persistent phenotypic changes at the level of gene transcription, i.e. neuroplasticity. Some of the known mechanisms that underlie this modulation are reviewed here.