OBJECTIVE: 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. METHODS: 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). RESULTS: 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. CONCLUSION: 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.
OBJECTIVE: 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. METHODS: 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). RESULTS: 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. CONCLUSION: 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.