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| Research article summary (published 30 Mar 2009): |
Gene-environmental interaction in the development of atopic asthma: new developments.
Full Abstract
PURPOSE OF REVIEW: Over recent years, major advances have occurred in understanding of the role of atopy in asthma. To accommodate these advances requires a revision in the paradigm that asthma is an atopic disease. In turn, a revision in the focus of gene-environment studies is now needed. The aim of this review, therefore, is to provide a new perspective to the topic of the role of genes and environment in the development of symptoms in atopic asthma. RECENT FINDINGS: Recent data from prospective birth-cohort studies has shown that atopic events appear to play a limited role in the development of asthma and even less of a role in significant acute wheeze in children. Overwhelmingly, acute respiratory viral infection, not acute allergen exposure, is the major environmental cause of acute wheezing episodes in asthmatic children. This knowledge has led to the examination of the genetics of the immune system, particularly genes controlling innate immune responses, with respect to viral defences - an important area of gene-environment interaction in asthma. SUMMARY: Advances in knowledge of the genetics of viral defence have contributed to improved insight into asthma in children and could lead to effective new antiviral asthma therapies.
Author information
Author/s: Le Souëf, Peter N (PN);
Affiliation: University of Western Australia, Perth, Australia. plesouef(-atsign-)meddent.uwa.edu.au
Journal and publication information
Publication Type: Journal Article; Review
Journal: Current opinion in allergy and clinical immunology (Curr Opin Allergy Clin Immunol), published in United States. (Language: eng)
Reference: 2009-Apr; vol 9 (issue 2) : pp 123-7
Dates: Created 2009/03/24; Completed 2009/05/14;
PMID: 19295429, status: MEDLINE (last retrieved date: 5/14/2009)
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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Associated Chemicals: HLX protein, human (0) ; Homeodomain Proteins (0) ; Interferon Regulatory Factor-1 (0) ; KCNMB1 protein, human (0) ; Large-Conductance Calcium-Activated Potassium Channel beta Subunits (0) ; Toll-Like Receptors (0) ; Transcription Factors (0)Related articles
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