Gene-environment interactions in chronic pulmonary diseases.
The increasing prevalence of asthma and other environmentally induced chronic pulmonary diseases is an important public health concern. It is now generally recognized that the aetiology of these diseases involves a complex interplay between genetic background and exposure to multiple environmental stimuli. This represents a major challenge for the development of new strategies for lung disease prevention and treatment. The completion of the Human Genome Project, the HapMap project, technological advances in genotyping, and the potential of genome-wide association analysis has led to a rapid increase in the number of suggested susceptibility genes for asthma and other environmentally induced chronic pulmonary diseases. The genetic studies have used two major methods, i.e., mapping techniques that pinpoint gene loci and studies that identify genes and polymorphisms associated with various asthma mechanisms such as inflammatory mediators. Because the formation of reactive oxygen species is a major aspect of the inflammatory process of the chronic pulmonary diseases, genetic aberrations associated with detoxification enzymes may also shed light on reasons why some people with chronic pulmonary diseases seem more at-risk of exacerbations as a result of environmental insults. This review summarises the present knowledge on the most intriguing potential candidate genes as modifiers of individual susceptibility to these complex diseases.
Hirvonen
Ari
A
Finnish Institute of Occupational Health, Topeliuksenkatu 41 a A, FIN-00250 Helsinki, Finland. ari.hirvonen@ttl.fi
D000393:Air Pollutants / Q000633:toxicity; D002908:Chronic Disease; D004777:Environment; D020022:Genetic Predisposition to Disease; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D008171:Lung Diseases / Q000209:etiology* / Q000235:genetics*; D010447:Peptide Hydrolases / Q000235:genetics; D012307:Risk Factors; D015262:Xenobiotics / Q000378:metabolism
D000393:Air Pollutants; D018836:Inflammation Mediators; D015262:Xenobiotics; D010447:Peptide Hydrolases