Polymorphisms of interleukin-10 and its receptor and lung function in COPD

¹ The James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, St. Paul's Hospital, University of British Columbia, Vancouver, B.C., Canada
² Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis, Minnesota, USA
³ Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada

^* To whom correspondence should be addressed. E-mail: asandford{at}mrl.ubc.ca.

	Abstract

Interleukin-10 (IL10) is a Th2 cytokine with a wide spectrum of anti-inflammatory actions. Inflammation plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). We hypothesized that single nucleotide polymorphisms (SNPs) of IL10 and its receptor (IL10RA) are associated with change or level of forced expiratory volume in one second (FEV₁), in smoking-induced COPD.

Eleven SNPs of IL10 and IL10RA were studied in 586 whites who had the fastest (n=280) or the slowest (n=306) decline of FEV₁ selected from among continuous smokers followed for 5 years in the Lung Health Study (LHS). These 11 SNPs were also studied in 1072 participants with the lowest (n=538) or the highest (n=534) baseline FEV₁ at the beginning of the LHS.

No association was found in the primary analyses. Although a subgroup analysis showed that the IL10_3368A allele was associated with fast decline of FEV₁ (p=0.02 for the additive model), the association did not pass correction for multiple comparisons. No gene-gene interaction of IL10 with IL10RA was found.

There was no association of IL10 and IL10RA polymorphisms with rate of decline or level of FEV₁ in smoking-induced COPD.

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