The Late Asthmatic ResponseLate stimulus and for many reasons is thought to resemble more closely the problems for which patients seek assistance than the immediate asthmatic response (IAR) that occurs within minutes of challenge. For example, the airway obstruction produced during LAR may be more severe and prolonged than that associated with IAR. In addition, the IAR may be easily reversed with inhaled or injected adrenergic drugs, while the LAR is less responsive to this form of therapy. While pretreatment with cromolyn prevents both IAR and LAR, corticosteroids given just before antigen exposure will not prevent LAR but will abolish or diminish LAR. The LAR has also been noted to correlate with frequent attacks of asthma and under laboratory conditions may occur in as many as 50 percent of challenged subjects. LARs that occur after either laboratory or natural exposure to antigen have been associated with subsequent increases in airways reactivity. This finding has led to the hypothesis that atopic asthmatic patients with LARs may develop a vicious circle in which heightened airway reactivity leads to enhanced responsiveness to allergens and nonimmunologic stimuli such as irritants and exercise, thus producing more persistent symptoms of asthma.

This review presents current thoughts on possible mechanisms that lead to the LAR. While the focus is on the antigen-induced LAR, observations of late phase reactions in the skin (late cutaneous response) and upper airways (late nasal response) that may give clues to the immunopathogen-esis of late phase reactions in the lung are also cited.

Importance of Antigen-Specific IgE in Antigen-Induced LAR
Studies by Pepys et al in patients with allergic bronchopulmonary aspergillosis and late reactions in skin and lung led to the hypothesis that late reactions were Arthus phenomena. However, recent studies of late phase reactions in the skin suggest that events with this time course are not necessarily type 3 events. For example, Solley and associates reported heating of atopic human serum used for passive sensitization reduced the capacity to transfer immediate and late cutaneous responses. Removal of IgE by passing the serum over an anti-IgE immunoabsorbent abolished the ability to transfer the reactions, while IgE from the immunoabsorbent restored the responses.

Late stimulus and for many reasons is thought to resemble more closely the problems for which patients seek assistance than the immediate asthmatic response (IAR) that occurs within minutes of challenge. For example, the airway obstruction produced during LAR may be more severe and prolonged than that associated with IAR. In addition, the IAR may be easily reversed with inhaled or injected adrenergic drugs, while the LAR is less responsive to this form of therapy. While pretreatment with cromolyn prevents both IAR and LAR, corticosteroids given just before antigen exposure will not prevent LAR but will abolish or diminish LAR. The LAR has also been noted to correlate with frequent attacks of asthma and under laboratory conditions may occur in as many as 50 percent of challenged subjects. LARs that occur after either laboratory or natural exposure to antigen have been associated with subsequent increases in airways reactivity. This finding has led to the hypothesis that atopic asthmatic patients with LARs may develop a vicious circle in which heightened airway reactivity leads to enhanced responsiveness to allergens and nonimmunologic stimuli such as irritants and exercise, thus producing more persistent symptoms of asthma.