MECHANISMS OF AIR-FLOW LIMITATION IN THE NOSE AND LUNGS

Authors
Citation
R. Dahl et N. Mygind, MECHANISMS OF AIR-FLOW LIMITATION IN THE NOSE AND LUNGS, Clinical and experimental allergy, 28, 1998, pp. 17-25
Citations number
72
Categorie Soggetti
Allergy,Immunology
ISSN journal
09547894
Volume
28
Year of publication
1998
Supplement
2
Pages
17 - 25
Database
ISI
SICI code
0954-7894(1998)28:<17:MOALIT>2.0.ZU;2-9
Abstract
The main differences in the anatomies of the upper and lower airways a re the vascular characteristics and bony surroundings of the upper air ways compared with the smooth muscle component and the loose-lying sit uation of the lower airways. Both allergic asthma and rhinitis involve a similar process of mucosal inflammation in response to allergen exp osure, characterized by inflammatory cell infiltration and local relea se of mediators. In addition, both the upper and lower airways are und er similar influences from local neuronal reflexes, exercise, posture and cyclic variations. Challenge tests have been able to demonstrate t he roles of the various influences and components in the inflammatory processes of asthma and allergic rhinitis. A particular difference in the response in asthma compared with rhinitis is the degree of non-spe cific hyperresponsiveness, which is a characteristic of the late respo nse or response to repeated or prolonged exposure to allergen. Respons iveness of the bronchial mucose in asthma patients is approximate to 5 0 times that of normal (nan-allergic or nonasthmatic) subjects, wherea s that of the nasal mucosa in allergic rhinitis is only 2-8 times that of control subjects. The inflammatory process involved in hyperrespon siveness is similar in both conditions, involving increased infiltrati on of eosinophils and subsequent increased mediator release. The great er degree of hyperresponsiveness seen in asthma appears to be a conseq uence of the anatomical differences between the upper vs the lower air ways. Evidence is presented for the contribution of increased airway w all thickness to the hyperresponsiveness in asthma, together with othe r possible factors, such as decoupling of responder tissue from surrou nding tissue, increased smooth muscle contractility, and smooth muscle hypertrophy.