Polymorphisms of interleukin-10 and its receptor and lung function in COPD
1The James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, St. Paul's Hospital, University of British Columbia, 1081 Burrard Street Vancouver, BC, V6Z 1Y6, Canada.
The European Respiratory Journal
|March 3, 2007
Summary
Genetic variations in Interleukin-10 (IL-10) and its receptor (IL10RA) were not linked to lung function decline in smokers with chronic obstructive pulmonary disease (COPD). This study found no significant association between IL-10/IL10RA gene polymorphisms and COPD progression.
Area of Science:
- Genetics
- Immunology
- Pulmonology
Background:
- Interleukin-10 (IL-10) is a cytokine with significant anti-inflammatory properties.
- Inflammation is a key factor in the development of chronic obstructive pulmonary disease (COPD).
Purpose of the Study:
- To investigate the association between single nucleotide polymorphisms (SNPs) in the IL-10 and IL10RA genes and lung function (FEV1) in smokers with COPD.
- To determine if genetic variations in IL-10 and IL10RA influence the rate of FEV1 decline or baseline FEV1 values.
Main Methods:
- Eleven SNPs in the IL10 and IL10RA genes were analyzed in 586 White subjects from the Lung Health Study with rapid or slow FEV1 decline.
- The same SNPs were examined in 1,072 participants with the lowest or highest baseline FEV1.
- Subjects were continuous smokers followed for 5 years.
Main Results:
- No significant association was found between the studied IL10 and IL10RA SNPs and FEV1 decline or baseline FEV1 in the primary analysis.
- A potential association of the IL-10 3368A allele with fast FEV1 decline was observed in a subgroup but did not withstand correction for multiple comparisons.
- No gene-gene interactions between IL10 and IL10RA were identified.
Conclusions:
- Polymorphisms in the genes encoding Interleukin-10 and its receptor alpha subunit are not associated with the rate of FEV1 decline or FEV1 values in smoking-induced COPD.
- These genetic factors do not appear to play a significant role in the progression of COPD in this cohort.
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