What is the pathophysiology of allergic rhinitis?

Updated: Jul 26, 2021
  • Author: Quoc A Nguyen, MD; Chief Editor: Arlen D Meyers, MD, MBA  more...
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Because the nose is the most common port of entry for allergens, in patients with allergies, signs and symptoms of allergic rhinitis, not surprisingly, are the most common complaints.

Four types of hypersensitivity responses exist, as initially classified by Gell and Coombs and later modified by Shearer and Huston. Individuals with allergic rhinitis are thought to have type I reactions.

After initial exposure to an antigen, antigen-processing cells (macrophages) present the processed peptides to T helper cells. Upon subsequent exposure to the same antigen, these cells are stimulated to differentiate into either more T helper cells or B cells. The B cells may further differentiate into plasma cells and produce immunoglobulin E (IgE) specific to that antigen. Allergen-specific IgE molecules then bind to the surface of mast cells, sensitizing them.

Further exposures result in the bridging of 2 adjacent IgE molecules, leading to the release of preformed mediators from mast cell granules. These mediators (ie, histamine, leukotrienes, kinins) cause early-phase symptoms such as sneezing, rhinorrhea, and congestion. Late-phase reactions begin 2-4 hours later and are caused by newly arrived inflammatory cells. Mediators released by these cells prolong the earlier reactions and lead to chronic inflammation.

A study by Shahsavan et al found that patients with moderate to severe persistent allergic rhinitis demonstrated significantly greater interleukin 22 (IL-22) and IL-17A production than did healthy controls, suggesting that the development of persistent allergic rhinitis is influenced by these cytokines. Moreover, a correlation was found between IL-22 and IL-17A serum levels, along with the mean number of IL-22– and IL-17A–positive cells in the nasal mucosa, and specific IgE levels, nasal eosinophil count, and total nasal symptom score (TNSS). [3]

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