Mediators of Inflammation in the Early and the Late Phase of Allergic Rhinitis

Inga Hansen; Ludger Klimek; Ralph Mösges; Karl Hörmann

Disclosures

Curr Opin Allergy Clin Immunol. 2004;4(3) 

In This Article

Early-Phase Response

When continuous allergen exposure takes place, increasing numbers of IgE-coated mast cells traverse the epithelium. IgE binds to the high-affinity IgE receptor (FcεRI) on tissue mast cells. Mast cell degranulation is triggered by the binding of bound IgE to FcεRI.[3,4] Degranulation releases preformed mediators such as histamine, tryptase, chymase, kininogenase (which generates bradykinin), or heparin. Conversely, mast cells secrete different inflammatory mediators de novo, such as prostaglandin D2 and the sulfidopeptidyl leukotrienes C4, D4 and E4. The latter, as bradykinin, cause blood vessels to broaden and leak and thus lead to the clinically important mucosal edema and the watery rhinorrhea. Furthermore, numerous cytokines are transcribed, such as tumor necrosis factor (TNF).[5]

The binding of IgE to FcεRI on basophils is followed by cross-linking by allergen, and results in basophil degranulation. Preformed mediators are released, and lipid mediators and cytokines are synthesized.[6]

Mucosal glands secrete mucoglycoconjugates and antimicrobial compounds and dilate blood vessels, leading to sinusoidal filling and thus to nasal congestion. The mediators, however, also stimulate sensory nerves, which produce the symptoms of nasal itching and congestion. Systemic reflexes such as sneezing are induced.

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