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Transforming growth factor-beta1 polymorphisms, airway responsiveness and lung function decline in smokers
Emiko Ogawa1, Jian Ruan, John E Connett
1James Hogg iCAPTURE Center for Cardiovascular and Pulmonary Research, St. Paul's Hospital, Room 166, 1081 Burrard Street, Vancouver, BC, Canada V6Z 1Y6.
Respiratory Medicine
|October 31, 2006
Summary
Genetic variations in transforming growth factor-beta1 (TGF-beta1) were studied in relation to chronic obstructive pulmonary disease (COPD). The TGF-beta1 +869 polymorphism may influence airway hyperresponsiveness but not the rate of lung function decline in smokers.
Area of Science:
- Pulmonary Medicine
- Genetics
- Inflammation Research
Background:
- Chronic obstructive pulmonary disease (COPD) involves airway inflammation and fibrosis, potentially linked to transforming growth factor-beta1 (TGF-beta1).
- Elevated TGF-beta1 levels are observed in the airways of COPD patients, suggesting a role in disease progression.
Purpose of the Study:
- To investigate the association between TGF-beta1 gene polymorphisms and the rate of forced expiratory volume in 1s (FEV(1)) decline in smokers.
- To explore the potential link between TGF-beta1 polymorphisms and airway hyperresponsiveness.
Main Methods:
- Genotyping of three TGF-beta1 polymorphisms (-509, +869, +915) in 590 smokers from the NHLBI Lung Health Study.
- Analysis of genotype distribution in relation to rapid versus slow FEV(1) decline and methacholine responsiveness.
Main Results:
- No significant association was found between the studied TGF-beta1 polymorphisms and the rate of FEV(1) decline.
- A significant difference in genotype distribution at the +869 locus was observed between high and low responders to methacholine (P=0.04).
Conclusions:
- The T-C polymorphism at position +869 in the TGF-beta1 gene appears to contribute to airway hyperresponsiveness.
- These TGF-beta1 polymorphisms are not associated with an accelerated rate of lung function decline in COPD patients.
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