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Asthma and chronic obstructive pulmonary disease: common genes, common environments?
Dirkje S Postma1, Marjan Kerkhof, H Marike Boezen
1Department of Pulmonology, University Medical Center Groningen, Hanzeplein 1, PO Box 30001, 9700 RB Groningen, The Netherlands. d.s.postma@long.umcg.nl
American Journal of Respiratory and Critical Care Medicine
|February 8, 2011
Summary
Genetic and environmental factors interact to influence the development of asthma and chronic obstructive pulmonary disease (COPD). Early life lung development genes, combined with exposures like smoking, contribute to both conditions, potentially enabling personalized therapies.
Area of Science:
- Pulmonary Medicine
- Genetics
- Environmental Health
Background:
- Asthma and COPD share genetic and environmental risk factors, including allergens, infections, and smoking.
- The Dutch hypothesis suggests disease development depends on the timing and type of environmental exposures interacting with genetic predispositions.
- Both unique and shared genetic factors, alongside common host and environmental risks, contribute to asthma and COPD.
Purpose of the Study:
- To propose that genes influencing early lung development interact with environmental stimuli to cause childhood asthma and adult COPD.
- To explore how additional genetic and environmental factors drive specific immunological mechanisms in asthma and COPD subtypes.
- To suggest that genetic predisposition can define patient subgroups for targeted therapies.
Main Methods:
- Review of existing data on genetic and environmental risk factors for asthma and COPD.
- Analysis of the proposed interaction between early-life lung development genes and environmental exposures.
- Examination of genetic contributions to distinct immunological pathways and COPD subtypes.
Main Results:
- Genes affecting in utero and early childhood lung development, interacting with stimuli like smoking and pollution, contribute to asthma and COPD.
- Specific genes and environmental factors drive distinct immunological pathways for asthma and contribute to COPD subtypes (e.g., emphysema, airway disease).
- Genetic predisposition may help define subgroups within asthma and COPD.
Conclusions:
- A unified genetic-environmental model explains the development of asthma and COPD, highlighting early life influences.
- Understanding these interactions can lead to better patient stratification based on genetic makeup.
- This approach may pave the way for novel therapeutic strategies for asthma and COPD.
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