title: Inflammatory mediators in allergic rhinitis.
abstract: 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.
authors.affiliation: Division of Cell Biology, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO, USA.
authors.forename: Erwin W
authors.initials: EW
authors.lastname: Gelfand
mesh_terms: D002940:Circadian Rhythm; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D012221:Rhinitis, Allergic, Perennial / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D018836:Inflammation Mediators