Unique mechanistic features of allergic rhinitis.

Symptoms of allergic rhinitis are produced by inflammatory mediators that are released upon activation of mast cells by antigen-IgE interaction. These mediators target the end organs directly or indirectly. Stimulation of sensory nerves by histamine, for example, leads to sneezing, pruritus, rhinorrhea, and nasal congestion. The clinical presentation of allergic rhinitis is also characterized by the phenomenon of hyperresponsiveness to nonallergic stimuli, such as cold air and various irritants. This phenomenon is believed to result from the effect of allergic inflammation on the sensory nerves that supply the upper airway mucosa. Various nonallergic triggers have been shown to act on the nasal mucosa through sensorineural stimulation. In allergic rhinitis, responsiveness to these stimuli is increased compared with the healthy state. A similar phenomenon is observed against such products of the allergic reaction as his-tamine and bradykinin. Also, in allergic rhinitis, stimulation of sensory nerves per se can produce inflammatory changes, a phenomenon known as neurogenic inflammation. The mechanism behind the development of sensorineural hyperresponsiveness and of increased propensity for neurogenic inflammation is unknown. However, evidence exists that the neurotrophin nerve growth factor, which can induce all these changes on sensory nerves, is produced in the human nasal mucosa and found in higher quantities in nasal secretions of patients with perennial allergic rhinitis as compared with healthy control subjects. Also, nerve growth factor is acutely released into nasal fluids after allergen provocation of patients with allergic disease. In patients with asthma of atopic origin, allergic rhinitis is almost ubiquitous. Because the nose is the air conditioner of the respiratory system, its dysfunction may negatively affect the lower airways. In addition to the conditioning of inhaled air, the association between allergic rhinitis and asthma may involve various mechanisms. For example, allergen provocation in the nose of a patient with asthma can lead to reductions in pulmonary function and to increased lower airway responsiveness after several hours. Also, nasal inflammation may propagate through a systemic route to affect the lower airways.