Genetics and Gene-Environment Interactions in Childhood and Adult Onset Asthma

被引:65
作者
Morales, Eva [1 ,2 ]
Duffy, David [3 ]
机构
[1] Univ Murcia, Biomed Res Inst Murcia IMIB Arrixaca, Murcia, Spain
[2] CIBER Epidemiol & Salud Publ CIBERESP, Madrid, Spain
[3] QIMR Berghofer Med Res Inst, Brisbane, Qld, Australia
关键词
asthma; genetics; environmental exposures; gene environment interactions; childhood; adulthood; GENOME-WIDE ASSOCIATION; AIR-POLLUTION EXPOSURE; S-TRANSFERASE P1; TOBACCO-SMOKE; LUNG-FUNCTION; RISK-FACTORS; ALLERGIC DISEASES; MATERNAL SMOKING; BRONCHIAL HYPERRESPONSIVENESS; ENDOTOXIN EXPOSURE;
D O I
10.3389/fped.2019.00499
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Asthma is a heterogeneous disease that results from the complex interaction between genetic factors and environmental exposures that occur at critical periods throughout life. It seems plausible to regard childhood-onset and adult-onset asthma as different entities, each with a different pathophysiology, trajectory, and outcome. This review provides an overview about the role of genetics and gene-environment interactions in these two conditions. Looking at the genetic overlap between childhood and adult onset disease gives one window into whether there is a correlation, as well as to mechanism. A second window is offered by the genetics of the relationship between each type of asthma and other phenotypes e.g., obesity, chronic obstructive pulmonary disease (COPD), atopy, vitamin D levels, and inflammatory and immune status; and third, the genetic-specific responses to the many environmental exposures that influence risk throughout life, and particularly those that occur during early-life development. These represent a large number of possible combinations of genetic and environmental factors, at least 150 known genetic loci vs. tobacco smoke, outdoor air pollutants, indoor exposures, farming environment, and microbial exposures. Considering time of asthma onset extends the two-dimensional problem of gene-environment interactions to a three-dimensional problem, since identified gene-environment interactions seldom replicate for childhood and adult asthma, which suggests that asthma susceptibility to environmental exposures may biologically differ from early life to adulthood as a result of different pathways and mechanisms of the disease.
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页数:14
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