ABSTRACT

The late response represents the secondary phase of an asthma episode, typically occurring 4 to 12 hours after the initial allergen induction in approximately 50% of all adults with extrinsic asthma and in 30% to 40% of patients with intrinsic asthma.5

Cytokines and other mediators cause adhesion molecules to form on the inner surface of bronchi and bronchioles, allowing inflammatory cells to attach to and enter the airway tissues. As early as 15 minutes after the initial insult, T-cells enter the airway tissue followed by eosinophils and basophils.1 These cells release mediators that are very similar to mast cells, causing airway narrowing secondary to progressive inflammation and mucus secretion. Inflammation causes the leakage of proteins into the airway tissues while the parasympathetic nervous system releases acetylcholine and causes bronchoconstriction. Once a late response is initiated in a patient with asthma, the patient is primed for future severe exacerbations as the inflammatory damage to the surface of airway cells exposes sensitive irritant receptors that can later be activated more easily upon future exposures to allergens or other stimuli.5