Over the next four to eight hours, the mediators released during the initial response set off a sequence of events, with enhanced inflammatory responses known as the late-phase response. In this phase, cytokines and various mediators released earlier promote the influx of other immune cells by enhancing expression of vascular cell adhesion molecules (VCAMs) that help traffic circulating eosinophils, neutrophils, and lymphocytes to the nasal endothelium. Although each of these cell types plays a role in the late response, eosinophils appear to be the main effector cell in allergic rhinitis. Nasal obstruction and secretions can lead to secondary effects, including ear and sinus infections, sleep apnea, and asthma exacerbations. Furthermore, the inflammmatory cytokines may circulate to the central nervous system, eliciting malaise, irritability, and impaired concentrations.
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