Interleukin-1β polymorphisms in Colombian patients with autoimmune rheumatic diseases

J. F. Camargo, P. A. Correa, J. Castiblanco, J. M. Anaya

Resultado de la investigación: Contribución a RevistaArtículo

67 Citas (Scopus)

Resumen

Interleukin-1 beta (IL-1β) exerts a range of inflammatory and immunomodulatory activities that are important in host defense and autoimmune response. The IL-1β gene, located on chromosome 2 (2q13), is polymorphic. The influence of its polymorphism on 355 patients with autoimmune rheumatic diseases was examined. To this effect, 172 patients with rheumatoid arthritis (RA), 114 with systemic lupus erythematosus (SLE), and 69 with primary Sjögren's syndrome (pSS) were studied. The control group consisted of 392 matched healthy individuals. Genotyping of IL-1β single-nucleotide polymorphisms (SNPs) at positions -511 (C/T) and + 3953 (C/T) was performed by the polymerase chain reaction-restriction fragment length polymorphism technique. In addition, levels of IL-1β were measured by immunoassay in supernatants of lipopolysaccharide (LPS)-stimulated and nonstimulated peripheral blood monocytes (PBM) obtained from 19 homozygous individuals for the three most common IL-1β likely haplotypes, all belonging to the control group. Allele + 3953T was protective for SLE (odds ratio (OR = 0.57, 95% confidence intervals (CI) = 0.34-0.88, P = 0.01) as was the haplotype -511C + 3953T (OR = 0.43, 95%CI = 0.25-0.74, pc = 0.006). The latter was associated with a lower LPS-stimulated-PBM IL-1β secretion. Results suggest that IL-1β polymorphism influences the susceptibility to acquire SLE in our population. The protective association might be explained by the observed inhibitory effect of IL-1β + 3953T allele on the secretion of IL-1β under inflammatory circumstances. © 2004 Nature Publishing Group All rights reserved.
Idioma originalEnglish (US)
Páginas (desde-hasta)609-614
Número de páginas6
PublicaciónGenes and Immunity
DOI
EstadoPublished - dic 1 2004

Huella dactilar

Rheumatic Diseases
Interleukin-1beta
Systemic Lupus Erythematosus
Autoimmune Diseases
Haplotypes
Lipopolysaccharides
Monocytes
Alleles
Confidence Intervals
Control Groups
Chromosomes, Human, Pair 2
Sjogren's Syndrome
Autoimmunity
Immunoassay
Restriction Fragment Length Polymorphisms
Single Nucleotide Polymorphism
Rheumatoid Arthritis
Odds Ratio
Polymerase Chain Reaction
Population

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title = "Interleukin-1β polymorphisms in Colombian patients with autoimmune rheumatic diseases",
abstract = "Interleukin-1 beta (IL-1β) exerts a range of inflammatory and immunomodulatory activities that are important in host defense and autoimmune response. The IL-1β gene, located on chromosome 2 (2q13), is polymorphic. The influence of its polymorphism on 355 patients with autoimmune rheumatic diseases was examined. To this effect, 172 patients with rheumatoid arthritis (RA), 114 with systemic lupus erythematosus (SLE), and 69 with primary Sj{\"o}gren's syndrome (pSS) were studied. The control group consisted of 392 matched healthy individuals. Genotyping of IL-1β single-nucleotide polymorphisms (SNPs) at positions -511 (C/T) and + 3953 (C/T) was performed by the polymerase chain reaction-restriction fragment length polymorphism technique. In addition, levels of IL-1β were measured by immunoassay in supernatants of lipopolysaccharide (LPS)-stimulated and nonstimulated peripheral blood monocytes (PBM) obtained from 19 homozygous individuals for the three most common IL-1β likely haplotypes, all belonging to the control group. Allele + 3953T was protective for SLE (odds ratio (OR = 0.57, 95{\%} confidence intervals (CI) = 0.34-0.88, P = 0.01) as was the haplotype -511C + 3953T (OR = 0.43, 95{\%}CI = 0.25-0.74, pc = 0.006). The latter was associated with a lower LPS-stimulated-PBM IL-1β secretion. Results suggest that IL-1β polymorphism influences the susceptibility to acquire SLE in our population. The protective association might be explained by the observed inhibitory effect of IL-1β + 3953T allele on the secretion of IL-1β under inflammatory circumstances. {\circledC} 2004 Nature Publishing Group All rights reserved.",
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Interleukin-1β polymorphisms in Colombian patients with autoimmune rheumatic diseases. / Camargo, J. F.; Correa, P. A.; Castiblanco, J.; Anaya, J. M.

En: Genes and Immunity, 01.12.2004, p. 609-614.

Resultado de la investigación: Contribución a RevistaArtículo

TY - JOUR

T1 - Interleukin-1β polymorphisms in Colombian patients with autoimmune rheumatic diseases

AU - Camargo, J. F.

AU - Correa, P. A.

AU - Castiblanco, J.

AU - Anaya, J. M.

PY - 2004/12/1

Y1 - 2004/12/1

N2 - Interleukin-1 beta (IL-1β) exerts a range of inflammatory and immunomodulatory activities that are important in host defense and autoimmune response. The IL-1β gene, located on chromosome 2 (2q13), is polymorphic. The influence of its polymorphism on 355 patients with autoimmune rheumatic diseases was examined. To this effect, 172 patients with rheumatoid arthritis (RA), 114 with systemic lupus erythematosus (SLE), and 69 with primary Sjögren's syndrome (pSS) were studied. The control group consisted of 392 matched healthy individuals. Genotyping of IL-1β single-nucleotide polymorphisms (SNPs) at positions -511 (C/T) and + 3953 (C/T) was performed by the polymerase chain reaction-restriction fragment length polymorphism technique. In addition, levels of IL-1β were measured by immunoassay in supernatants of lipopolysaccharide (LPS)-stimulated and nonstimulated peripheral blood monocytes (PBM) obtained from 19 homozygous individuals for the three most common IL-1β likely haplotypes, all belonging to the control group. Allele + 3953T was protective for SLE (odds ratio (OR = 0.57, 95% confidence intervals (CI) = 0.34-0.88, P = 0.01) as was the haplotype -511C + 3953T (OR = 0.43, 95%CI = 0.25-0.74, pc = 0.006). The latter was associated with a lower LPS-stimulated-PBM IL-1β secretion. Results suggest that IL-1β polymorphism influences the susceptibility to acquire SLE in our population. The protective association might be explained by the observed inhibitory effect of IL-1β + 3953T allele on the secretion of IL-1β under inflammatory circumstances. © 2004 Nature Publishing Group All rights reserved.

AB - Interleukin-1 beta (IL-1β) exerts a range of inflammatory and immunomodulatory activities that are important in host defense and autoimmune response. The IL-1β gene, located on chromosome 2 (2q13), is polymorphic. The influence of its polymorphism on 355 patients with autoimmune rheumatic diseases was examined. To this effect, 172 patients with rheumatoid arthritis (RA), 114 with systemic lupus erythematosus (SLE), and 69 with primary Sjögren's syndrome (pSS) were studied. The control group consisted of 392 matched healthy individuals. Genotyping of IL-1β single-nucleotide polymorphisms (SNPs) at positions -511 (C/T) and + 3953 (C/T) was performed by the polymerase chain reaction-restriction fragment length polymorphism technique. In addition, levels of IL-1β were measured by immunoassay in supernatants of lipopolysaccharide (LPS)-stimulated and nonstimulated peripheral blood monocytes (PBM) obtained from 19 homozygous individuals for the three most common IL-1β likely haplotypes, all belonging to the control group. Allele + 3953T was protective for SLE (odds ratio (OR = 0.57, 95% confidence intervals (CI) = 0.34-0.88, P = 0.01) as was the haplotype -511C + 3953T (OR = 0.43, 95%CI = 0.25-0.74, pc = 0.006). The latter was associated with a lower LPS-stimulated-PBM IL-1β secretion. Results suggest that IL-1β polymorphism influences the susceptibility to acquire SLE in our population. The protective association might be explained by the observed inhibitory effect of IL-1β + 3953T allele on the secretion of IL-1β under inflammatory circumstances. © 2004 Nature Publishing Group All rights reserved.

U2 - 10.1038/sj.gene.6364133

DO - 10.1038/sj.gene.6364133

M3 - Article

C2 - 15470475

SP - 609

EP - 614

JO - Genes and Immunity

JF - Genes and Immunity

SN - 1466-4879

ER -