Sensory and Autonomic Nervous System in Asthma and Rhinitis

Studies of nerve-immune interactions often focus onmechanisms by which the nervous system can modulateimmunity. With respect to inflammatory disease there hasbeen a longstanding interest in nerve-mediated (neurogenic)inflammation. In allergic airway disease, however, it may bemore useful to reverse the arrow of this interaction and evaluatethe neuronal consequence of IgE-mediated inflammation. Thischapter, in large part, focuses on this issue. Many of the signsand symptoms of allergic airway disease can be attributableto neural dysregulation. These include the self-evidentneuronal symptoms of itchy sensations, constant sneezing, drynonproductive coughing, inappropriate sensations of air hunger,as well as less conscious corruptions in autonomic reflexesincluding excessive secretions and inappropriate reflexbronchoconstriction. Moreover, the perceived triggers ofsymptoms in allergic rhinitis and asthma are often not onlyallergens but also emotions and inhalation of nonallergenicirritants. To explain this, one might logically hypothesize thatthe airway nervous system itself is a target of the allergicinflammatory reaction. In fact, in the laboratory, allergicinflammation has been shown to modulate all aspects of airwayinnervation, including modulation of the excitability of sensorynerve terminals, synaptic modulation in the central nervoussystem (CNS), and changes in activity of the autonomic airwayparasympathetic nerves. This modulation may involve acute andshort-lasting mechanisms, or long-lasting phenotypic changesin the nerves. This chapter provides an overview of airwayinnervation, how airway neurophysiology may change in theface of allergic inflammation, and how this may contribute toallergic airway diseases.