Late-phase inflammation: Influence on morbidity

With the prevalence of asthma and other allergic diseases increasing, the question of late-phase inflammatory response, a dynamic inflammatory response to a single exposure to antigen, has come to the forefront as one possible explanation for this increase in morbidity. If this explanation is acceptable, clinicians must examine their methods of management of allergic diseases and shift from crisis intervention with beta-agonists for asthma and first-generation antihistamines or decongestants for rhinitis to disease control with antiinflammatory agents. Topical application of corticosteroids to the upper airways blocks mediator release from the early and late phase after antigen challenges. In addition, recent studies using the skin-blister chamber model have shown that some of the newer, second-generation antihistamines may attenuate the infiltration and activation of eosinophils, neutrophils, and basophils during the late-phase response. Immunotherapy may have a selective effect, targeting inflammatory aspects of the late-phase response. It is clear that corticosteroids, second-generation antihistamines, and immunotherapy play a role in modifying the late-phase response and that each of these therapeutic modalities may operate by a different mechanism.