Non-atopic intrinsic asthma and the 'family tree' of chronic respiratory disease syndromes

Holt, P. G. and Sly, P. D. (2009) Non-atopic intrinsic asthma and the 'family tree' of chronic respiratory disease syndromes. Clinical And Experimental Allergy, 39 6: 807-811. doi:10.1111/j.1365-2222.2009.03258.x


Author Holt, P. G.
Sly, P. D.
Title Non-atopic intrinsic asthma and the 'family tree' of chronic respiratory disease syndromes
Journal name Clinical And Experimental Allergy   Check publisher's open access policy
ISSN 0954-7894
1365-2222
Publication date 2009-06
Sub-type Article (original research)
DOI 10.1111/j.1365-2222.2009.03258.x
Volume 39
Issue 6
Start page 807
End page 811
Total pages 5
Place of publication Oxford, United Kingdom
Publisher Wiley-Blackwell
Language eng
Abstract We present a scheme below in which the most common forms of inflammatory diseases of the respiratory tract, notably atopic and non-atopic asthma and COPD, are depicted as separate offshoots from a common ‘at-risk’ pathway underpinned by genotypes related to aberrations in control of host defence and tissue repair mechanisms. We propose that entrance into this pathway is initially programmed by environmental experience during infancy and early childhood, in particular by severe lower respiratory tract infection, and that further progression towards expression of specific disease phenotype(s) is determined by the nature, timing and frequency of additional environmental insults subsequently encountered. At the one extreme, early sensitization of at-risk subjects to aeroallergens can potentially drive rapid progression towards expression of the atopic asthmatic phenotype under the dual onslaught of inflammatory responses to allergens/pathogens. At the opposite end of the spectrum the drip-feed effects of occasional infections on respiratory function(s) are amplified over a longer time frame by inflammation resulting from exposure to tobacco smoke and/or related chemical pollutants. Non-atopic asthma is envisaged to fit between these two extremes, being driven essentially by the downstream effects of respiratory infections alone in at-risk subjects. An important common factor in all three disease phenotypes is that acute exacerbations are typically driven by infections, the host responses to which display a characteristic T-helper type 2-like footprint, which in our view points to underlying genotype(s) which result in unbalanced host responses to respiratory pathogens.
Keyword Obstructive Pulmonary-disease
Persistent Asthma
birth-cohort
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: Faculty of Health and Behavioural Sciences -- Publications
 
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Created: Wed, 17 Nov 2010, 11:32:03 EST