Inflammatory mediators in allergic rhinitis

Allergic rhinitis (AR) is part of a systemic disease complex. There is a close relationship between AR and asthma, which has led to the "one airway, one disease" concept. Both conditions share common immunopathology and pathophysiology. In patients with AR, allergen-triggered early and late responses are mediated by a series of inflammatory cells. Within minutes of contact with allergen, IgE-sensitized mast cells degranulate, releasing both preformed and newly synthesized mediators. Immunologic processes in both nasal and bronchial tissue involve T(H)2 lymphocytes and eosinophils. Eosinophils are the predominant cell in the chronic inflammatory process characteristic of the late-phase allergic response. Eosinophils release an array of proinflammatory mediators, including cysteinyl leukotrienes, cationic proteins, eosinophil peroxidase, and major basic protein, and might serve as a major source of IL-3, IL-5, GM-CSF, and IL-13. Neuropeptides also appear to contribute to the pathophysiology of AR symptoms. Both AR and asthma exhibit marked day-night variation in symptom severity. Acknowledging both the chronobiology of AR and circadian rhythm-dependent attributes of antiallergy medications might enhance the beneficial effects of allergy therapies. (J Allergy Clin Immunol 2004; 114: S135-8.)