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1 The James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, St. Pauls Hospital, University of British Columbia, Vancouver, BC, and 3 Faculty of Medicine, University of Manitoba, Winnipeg, MB, Canada. 2 Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis, MN, USA.
CORRESPONDENCE: A. J. Sandford, UBC James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, St. Pauls Hospital, 1081 Burrard Street Vancouver, BC, V6Z 1Y6, Canada. Fax: 1 6048068351. E-mail: asandford{at}mrl.ubc.ca
Keywords: Chronic obstructive pulmonary disease, forced expiratory volume in one second, genetic polymorphism, interleukin-10, interleukin-10 receptor
, lung function
Received: January 8, 2007
Accepted February 9, 2007
Interleukin (IL)-10 is a type-2 T-helper cell cytokine with a broad spectrum of anti-inflammatory actions. Inflammation plays an important role in the pathogenesis of chronic obstructive pulmonary disease. It was hypothesised that single nucleotide polymorphisms (SNPs) of the genes encoding IL-10 (IL10) and the
In total, eleven SNPs of IL10 and IL10RA were studied in 586 White subjects, selected from continuous smokers followed for 5 yrs in the Lung Health Study, who showed the fastest (n = 280) and slowest (n = 306) decline in FEV1. These 11 SNPs were also studied in 1,072 participants exhibiting the lowest (n = 538) and highest (n = 534) baseline FEV1 at the beginning of the Lung Health Study.
No association was found in the primary analyses. Although a subgroup analysis showed that the IL-10 3368A allele was associated with a fast decline in FEV1, the association did not pass correction for multiple comparisons. No genegene interaction of IL10 with IL10RA was found.
There was no association of polymorphisms of the genes encoding interleukin-10 and the
subunit of its receptor (IL10RA) are associated with changes in, or value of, forced expiratory volume in one second (FEV1) in smoking-induced chronic obstructive pulmonary disease.
subunit of its receptor with the rate of decline in, or value of, forced expiratory volume in one second in smoking-induced chronic obstructive pulmonary disease.
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