Airway hyperresponsiveness is an important feature of clinical asthma. This means that asthmatic patients will develop bronchoconstriction after inhaling a smaller concentration of a bronchoconstrictor agonist (usually 10-100 times less) than is needed to induce the same degree of bronchoconstriction in nonasthmatic subjects. Airway hyperresponsiveness is not only an objective measurement which can distinguish asthmatic from normal subjects, but also the degree of airway hyperresponsiveness is related to the severity of asthma, and to the amount of treatment needed to optimally control symptoms.
In many asthmatic subjects, airway hyperresponsiveness is a stable phenomenon when measured over several years; however, in some subjects, airway responsiveness can be increased after exposure to inhaled allergens, ozone, upper respiratory tract infections or occupational sensitizing agents. This increase in airway responsiveness is associated with increased symptoms of asthma. All of these stimuli are naturally occurring stimuli; however, allergen, ozone and occupational sensitizing agents such as toluene diisocyanate (TDI) have been used in both human and animal preparations to study the pathogenesis of airway hyperresponsiveness in the research laboratory.