Interleukin 1 and nuclear factor-kappaB polymorphisms in ankylosing spondylitis in Canada and Korea

The interleukin 1alpha and 1beta (IL-1alpha, IL-1beta) are potent mediators of inflammation and immunity. IL-1 receptor antagonist (IL-1Ra) is a protein that binds to IL-1 receptors and competitively inhibits the binding of IL-1alpha and IL-1beta. There are reports of IL-1 complex gene polymorphisms in ankylosing spondylitis (AS), but the results have been inconsistent. NFKB1 encodes the genes for the p50 and p101 nuclear factor-kappaB (NF-kappaB) isoforms, which are recognized as critical to inflammatory disease. To date there have been no reports examining an association between NFKB1 and AS. We investigated polymorphisms of IL-1 complex and NF-kappaB1 with 2 genetically and geographically different populations.

Subjects with AS satisfied modified New York criteria for AS. Healthy controls were recruited at each respective site. Subjects with AS were genotyped for the following: IL-1alpha-889 single nucleotide polymorphism (SNP); IL-1beta +3953 SNP; IL-1Ra (86 base pair variable number tandem repeat within intron 2); and NFKB1 (-94 insertion/deletion polymorphism).

In total, 205 subjects with AS and 200 controls from Seoul, Korea, and 68 subjects with AS and 164 controls from Toronto, Canada, were genotyped for the IL-1alpha and IL-1beta polymorphisms and 115 controls for the IL-1Ra and NF-kappaB polymorphisms. There were no differences of IL-1alpha, IL-1beta, IL-1Ra, and NF-kappaB polymorphisms between AS patients and controls in these populations.

Our analysis of these SNP in the IL-1 complex and NF-kappaB genes does not support a major role for either in AS susceptibility in the Seoul and Toronto populations.