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

T H Kim, M A Stone, P Rahman, D H Yoo, Y W Park, U Payne, D Hallett, R D Inman

Research output: Contribution to journalArticle

Abstract

Objective. The interleukin 1 alpha and 1 beta (IL-1 alpha, IL-1 beta) 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-1 alpha and IL-1 beta. 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-KB (NF-kappa B) 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-kappa B1 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-1 alpha-889 single nucleotide polymorphism (SNP); IL-1 beta +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-1 alpha and IL-1 beta polymorphisms and 115 controls for the IL-1R alpha and NF-kappa B polymorphisms. There were no differences of IL-1 alpha, IL-1 beta, IL-1Ra, and NF-kappa B polymorphisms between AS patients and controls in these populations. Conclusion. Our analysis of these SNP in the IL-1 complex and NF-kappa B genes does not support a major role for either in AS susceptibility in the Seoul and Toronto populations.
LanguageEnglish
Pages1907-1910
Number of pages4
JournalJournal of Rheumatology
Volume32
Issue number10
StatusPublished - 2005

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NF-kappa B
Ankylosing Spondylitis
Korea
Interleukin-1
Canada
Interleukin-1alpha
Interleukin-1beta
Interleukin-1 Receptors
Single Nucleotide Polymorphism
Population
Genes
Inflammation Mediators
Minisatellite Repeats
Base Pairing
Introns
Immunity
Protein Isoforms

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Kim, T. H., Stone, M. A., Rahman, P., Yoo, D. H., Park, Y. W., Payne, U., ... Inman, R. D. (2005). Interleukin 1 and nuclear factor-kappa B polymorphisms in ankylosing spondylitis in Canada and Korea.

Interleukin 1 and nuclear factor-kappa B polymorphisms in ankylosing spondylitis in Canada and Korea. / Kim, T H; Stone, M A; Rahman, P; Yoo, D H; Park, Y W; Payne, U; Hallett, D; Inman, R D.

In: Journal of Rheumatology, Vol. 32, No. 10, 2005, p. 1907-1910.

Research output: Contribution to journalArticle

Kim, TH, Stone, MA, Rahman, P, Yoo, DH, Park, YW, Payne, U, Hallett, D & Inman, RD 2005, 'Interleukin 1 and nuclear factor-kappa B polymorphisms in ankylosing spondylitis in Canada and Korea' Journal of Rheumatology, vol. 32, no. 10, pp. 1907-1910.
Kim TH, Stone MA, Rahman P, Yoo DH, Park YW, Payne U et al. Interleukin 1 and nuclear factor-kappa B polymorphisms in ankylosing spondylitis in Canada and Korea. Journal of Rheumatology. 2005;32(10):1907-1910.
Kim, T H ; Stone, M A ; Rahman, P ; Yoo, D H ; Park, Y W ; Payne, U ; Hallett, D ; Inman, R D. / Interleukin 1 and nuclear factor-kappa B polymorphisms in ankylosing spondylitis in Canada and Korea. In: Journal of Rheumatology. 2005 ; Vol. 32, No. 10. pp. 1907-1910
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abstract = "Objective. The interleukin 1 alpha and 1 beta (IL-1 alpha, IL-1 beta) 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-1 alpha and IL-1 beta. 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-KB (NF-kappa B) 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-kappa B1 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-1 alpha-889 single nucleotide polymorphism (SNP); IL-1 beta +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-1 alpha and IL-1 beta polymorphisms and 115 controls for the IL-1R alpha and NF-kappa B polymorphisms. There were no differences of IL-1 alpha, IL-1 beta, IL-1Ra, and NF-kappa B polymorphisms between AS patients and controls in these populations. Conclusion. Our analysis of these SNP in the IL-1 complex and NF-kappa B genes does not support a major role for either in AS susceptibility in the Seoul and Toronto populations.",
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AU - Payne,U

AU - Hallett,D

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N2 - Objective. The interleukin 1 alpha and 1 beta (IL-1 alpha, IL-1 beta) 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-1 alpha and IL-1 beta. 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-KB (NF-kappa B) 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-kappa B1 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-1 alpha-889 single nucleotide polymorphism (SNP); IL-1 beta +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-1 alpha and IL-1 beta polymorphisms and 115 controls for the IL-1R alpha and NF-kappa B polymorphisms. There were no differences of IL-1 alpha, IL-1 beta, IL-1Ra, and NF-kappa B polymorphisms between AS patients and controls in these populations. Conclusion. Our analysis of these SNP in the IL-1 complex and NF-kappa B genes does not support a major role for either in AS susceptibility in the Seoul and Toronto populations.

AB - Objective. The interleukin 1 alpha and 1 beta (IL-1 alpha, IL-1 beta) 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-1 alpha and IL-1 beta. 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-KB (NF-kappa B) 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-kappa B1 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-1 alpha-889 single nucleotide polymorphism (SNP); IL-1 beta +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-1 alpha and IL-1 beta polymorphisms and 115 controls for the IL-1R alpha and NF-kappa B polymorphisms. There were no differences of IL-1 alpha, IL-1 beta, IL-1Ra, and NF-kappa B polymorphisms between AS patients and controls in these populations. Conclusion. Our analysis of these SNP in the IL-1 complex and NF-kappa B genes does not support a major role for either in AS susceptibility in the Seoul and Toronto populations.

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