Atopy predisposes an individual to the development of asthma, whereby specific triggers may repeatedly cause acute exacerbations and contribute to chronic inflammation. This IgE-mediated response to common allergens is the strongest predisposing factor for developing asthma. Airway inflammation involves release of immunological mediators via T lymphocyte dependent, and IgE dependent and independent mechanisms which attract inflammatory cells from the circulation. The role of the eicosanoids as pivotal mediators in promoting some of the changes in asthma has only recently been fully explored. Inflammatory reactions result when mediators and cytokines released from resident and infiltrating cells interact. This interaction also contributes to the bronchoconstriction, hypersecretion, and mucosal edema in the airways.
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