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Non specific airway responsiveness

Following natural antigenic exposure, NSAR can increase in non asthmatic subjects with allergic rhinitis, although it may not reach the "hyperresponsive range", and is associated with the development of a cough. Natural exposure in non-asthmatic atopics may induce an inflammatory reaction in the airways to a degree that may increase NSAR[1].

Nonspecific airway hyperresponsiveness (AHR), a cardinal feature of asthma, is thought to result from several genetic and environmental factors. Asymptomatic AHR in nonasthmatic healthy subjects might be a risk factor for the development of asthma. Genetic variations in codons 16 and 27 of the human beta(2)-adrenergic receptor (beta(2)-AR) alter receptor function in vitro and are associated with various asthma-related phenotypes, including asthma severity and AHR. This study indicates that a specific beta(2)-AR polymorphism at codon 16 might be a genetic determinant of AHR, as judged by methacholine-induced bronchoconstriction in asymptomatic healthy subjects.

 

References

1.Boulet, L. - P. et al: Bronchial responsiveness increases after seasonal antigen exposure in non-asthmatic subjects with pollen-induced rhinitis. Ann. Allergy (1989) 63, No.2, p. 114.


2.Fukui Y, Hizawa N, Takahashi D, Maeda Y, Jinushi E, Konno S, Nishimura M. Association between nonspecific airway hyperresponsiveness and Arg16Gly beta2-adrenergic receptor gene polymorphism in asymptomatic healthy Japanese subjects.Chest. 2006 Aug;130(2):449-54.

Γκέλης Ν.Δ. - Λεξικό Αλλεργίας - Εκδόσεις ΒΕΛΛΕΡOΦΟΝΤΗΣ - Κόρινθος 2013

Gelis Ν.D. - Dictionary of Allergies - VELLEROFONTIS Publications - Corinth 2013