Measuring airway responsiveness to inhaled bronchoconstrictor stimuli, such
as methacholine or histamine, has become an important tool in the diagnosi
s of asthma. This is measured by patients inhaling increasing doses or conc
entrations of the bronchoconstrictor stimulus until a given level of bronch
oconstriction is achieved. Inhaled allergens initiate processes that increa
se airway inflammation and enhance airway hyperresponsiveness in asthmatic
subjects. Studies using inhaled allergen challenges have provided insight i
nto how changes in airway hyperresponsiveness are regulated by induced infl
ammatory processes. These changes in airway hyperresponsiveness (1-2 doubli
ng doses) have been shown to be of much smaller magnitude than those demons
trated when asthmatics with stable airway hyperresponsiveness are compared
to normals (4-8 doubling doses). These allergen-induced changes would be of
little relevance in subjects with normal airway responsiveness, because th
ey would not increase the degree of airway responsiveness into the asthmati
c range. They are, however, important in asthmatics who already have airway
hyperresponsiveness because they are similar to changes associated with wo
rsening asthma control. It is likely that the mechanisms responsible for th
e changes in airway hyperresponsiveness following experimental allergen exp
osure are similar to those producing transient worsening of control in asth
matics. Nevertheless, it is unlikely that the mechanisms of the transient a
llergen-induced airway hyperresponsiveness will explain the underlying mech
anisms of the persistent airway hyperresponsiveness in asthmatic patients w
hen compared with normal individuals.