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Pathogenesis of allergic rhinitis (rhinosinusitis)

Richard D deShazo, MD
Stephen F Kemp, MD
Section Editor
Jonathan Corren, MD
Deputy Editor
Anna M Feldweg, MD


Allergic rhinitis is associated with a symptom complex characterized by paroxysms of sneezing, rhinorrhea, nasal obstruction, and itching of the eyes, nose, and palate. It is also frequently associated with postnasal drip, cough, irritability, and fatigue [1-3].

The pathogenesis of allergic rhinitis is presented in this topic review. The clinical manifestations, diagnosis, and treatment of this condition are discussed separately. (See "Chronic rhinosinusitis: Clinical manifestations, pathophysiology, and diagnosis" and "Allergic rhinitis: Clinical manifestations, epidemiology, and diagnosis" and "Pharmacotherapy of allergic rhinitis".)


Upon exposure to an allergen, atopic individuals respond by producing allergen-specific immunoglobulin E (IgE). These IgE antibodies bind to IgE receptors on mast cells in the respiratory mucosa and to basophils in the peripheral blood. When the same allergen is subsequently inhaled, the IgE antibodies are bridged on the cell surface by allergen, resulting in activation of the cell. Mast cells in the nasal tissues release preformed and granule-associated chemical mediators, which cause the symptoms of allergic rhinitis.

Models of nasal allergen challenge in patients with allergic rhinitis have provided information about the pathogenesis of allergic rhinitis [4,5]. In this model study system, individuals known to have allergic rhinitis on exposure to a particular allergen are exposed to incremental doses of that allergen placed in the nose. The subsequent reaction is then monitored over time with nasal biopsies or washes. This allows direct quantitation of cell types by stains and surface markers, assessment of message for transcription, or direct measurement of cellular cytokines and other inflammatory mediators [6]. Rhinomanometry, the measurement of nasal airway resistance, permits measurement of both resistance and airflow following allergen provocative challenge [7]. (See "Occupational rhinitis", section on 'Rhinomanometry techniques'.)

Immunogenetics — The expression of allergic diseases of the upper airways reflects an autosomal-dominant pattern of inheritance with incomplete penetrance. This inheritance pattern is manifested as a propensity to respond to inhalant allergen exposure by producing high levels of allergen-specific IgE. The IgE response appears to be controlled by immune response genes located within the major histocompatibility complex (MHC) on chromosome 6. (See "Major histocompatibility complex (MHC) structure and function".)


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Literature review current through: Sep 2016. | This topic last updated: Jul 31, 2014.
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  1. Dykewicz MS, Fineman S, Skoner DP, et al. Diagnosis and management of rhinitis: complete guidelines of the Joint Task Force on Practice Parameters in Allergy, Asthma and Immunology. American Academy of Allergy, Asthma, and Immunology. Ann Allergy Asthma Immunol 1998; 81:478.
  2. Ng ML, Warlow RS, Chrishanthan N, et al. Preliminary criteria for the definition of allergic rhinitis: a systematic evaluation of clinical parameters in a disease cohort (I). Clin Exp Allergy 2000; 30:1314.
  3. Ng ML, Warlow RS, Chrishanthan N, et al. Preliminary criteria for the definition of allergic rhinitis: a systematic evaluation of clinical parameters in a disease cohort (II). Clin Exp Allergy 2000; 30:1417.
  4. Borish L. Allergic rhinitis: systemic inflammation and implications for management. J Allergy Clin Immunol 2003; 112:1021.
  5. Braunstahl GJ. The unified immune system: respiratory tract-nasobronchial interaction mechanisms in allergic airway disease. J Allergy Clin Immunol 2005; 115:142.
  6. Christodoulopoulos P, Cameron L, Durham S, Hamid Q. Molecular pathology of allergic disease. II: Upper airway disease. J Allergy Clin Immunol 2000; 105:211.
  7. Dunagan DP, Georgitis JW. Intranasal disease and provocation. In: Diagnostic testing of allergic disease, Kemp SF, Lockey RF (Eds), Marcel Dekker, 151 2000.
  8. Fokkens WJ. Antigen-presenting cells in nasal allergy. Allergy 1999; 54:1130.
  9. Godthelp T, Fokkens WJ, Kleinjan A, et al. Antigen presenting cells in the nasal mucosa of patients with allergic rhinitis during allergen provocation. Clin Exp Allergy 1996; 26:677.
  10. Chomarat P, Banchereau J. Interleukin-4 and interleukin-13: their similarities and discrepancies. Int Rev Immunol 1998; 17:1.
  11. Broide DH, Paine MM, Firestein GS. Eosinophils express interleukin 5 and granulocyte macrophage-colony-stimulating factor mRNA at sites of allergic inflammation in asthmatics. J Clin Invest 1992; 90:1414.
  12. Worm M, Henz BM. Molecular regulation of human IgE synthesis. J Mol Med (Berl) 1997; 75:440.
  13. Oettgen HC, Geha RS. IgE in asthma and atopy: cellular and molecular connections. J Clin Invest 1999; 104:829.
  14. Walls AF, He S, Buckley MG, McEuen AR. Roles of the mast cell and basophil in asthma. Clin Exp Allergy Rev 2001; 1:68.
  15. Haberal I, Corey JP. The role of leukotrienes in nasal allergy. Otolaryngol Head Neck Surg 2003; 129:274.
  16. Iwasaki M, Saito K, Takemura M, et al. TNF-alpha contributes to the development of allergic rhinitis in mice. J Allergy Clin Immunol 2003; 112:134.
  17. Cates EC, Gajewska BU, Goncharova S, et al. Effect of GM-CSF on immune, inflammatory, and clinical responses to ragweed in a novel mouse model of mucosal sensitization. J Allergy Clin Immunol 2003; 111:1076.
  18. Salib RJ, Kumar S, Wilson SJ, Howarth PH. Nasal mucosal immunoexpression of the mast cell chemoattractants TGF-beta, eotaxin, and stem cell factor and their receptors in allergic rhinitis. J Allergy Clin Immunol 2004; 114:799.
  19. Orban NT, Saleh H, Durham SR. Allergic and non-allergic rhinitis. In: Middleton's allergy: Principles and practice, 7th ed, Adkinson NF, Bochner BS, Busse WW, et al (Eds), Mosby, St. Louis 2009. p.973.
  20. Baraniuk JN. Pathogenesis of allergic rhinitis. J Allergy Clin Immunol 1997; 99:S763.
  21. Moqbel R, Levi-Schaffer F, Kay AB. Cytokine generation by eosinophils. J Allergy Clin Immunol 1994; 94:1183.
  22. Ponikau JU, Sherris DA, Kephart GM, et al. Striking deposition of toxic eosinophil major basic protein in mucus: implications for chronic rhinosinusitis. J Allergy Clin Immunol 2005; 116:362.
  23. Hanazawa T, Antuni JD, Kharitonov SA, Barnes PJ. Intranasal administration of eotaxin increases nasal eosinophils and nitric oxide in patients with allergic rhinitis. J Allergy Clin Immunol 2000; 105:58.
  24. Arnal JF, Didier A, Rami J, et al. Nasal nitric oxide is increased in allergic rhinitis. Clin Exp Allergy 1997; 27:358.
  25. Baroody FM, Naclerio RM. Allergic rhinitis. In: Clinical immunology. Principles and practice, 2nd ed, Rich RR, Fleisher TA, Shearer WT, et al (Eds), Mosby, London 2001. p.481.
  26. Hansen I, Klimek L, Mösges R, Hörmann K. Mediators of inflammation in the early and the late phase of allergic rhinitis. Curr Opin Allergy Clin Immunol 2004; 4:159.
  27. Baroody FM, Ford S, Proud D, et al. Relationship between histamine and physiological changes during the early response to nasal antigen provocation. J Appl Physiol (1985) 1999; 86:659.
  28. Naclerio RM, Proud D, Togias AG, et al. Inflammatory mediators in late antigen-induced rhinitis. N Engl J Med 1985; 313:65.
  29. Banov C, LaForce C, Lieberman P. Double blind trial of Astelin nasal spray in the treatment of vasomotor rhinitis. Ann Allergy Asthma Immunol 2000; 84:138.