Sinusitis, Rhinitis, Asthma, and the Single Airway Hypothesis

Abstract

The one airway, one disease hypothesis proposes that the upper and lower airways share the same physiology and histomorphology. Epidemiological clinical studies support a link between rhinosinusitis and asthma. The relationship can occur in both directions, with nasal allergen challenge leading to inflammatory changes in the lower airway and bronchoprovocation studies of the lower airway leading to inflammatory changes in the upper airway. In addition, both similarities and differences exist in the pathogenesis of nasal polyps and asthma. The mechanism for the connection between the upper and lower airways is a matter of great debate. It has been proposed that inflammatory changes in the lower airway may lead to systemic inflammatory effects that play a role in increased bronchial hyperresponsiveness. Similarly, lower airway inflammatory changes may affect nasal airway patency via systemic effects. Moreover, nasopharyngeal-bronchial reflexes may play a non-immunologic role in the interaction between the lower and upper airways. An example of the connection between the upper and lower airways is found in aspirin-exacerbated respiratory disease whereby leukotrienes play a role in the pathology of chronic rhinosinusitis with polyps and asthma. It is also been observed that the treatment of asthma is hindered by untreated rhinosinusitis.