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Evaluating the association of interleukin-10 gene promoter -592 A/C polymorphism with lupus nephritis susceptibility

BACKGROUND: Interleukin-10 (IL-10) is an important immunoregulatory cytokine. There are few studies evaluating the association between IL-10 and lupus nephritis (LN). The aim of this study was to evaluate the association of IL-10 gene promoter -592 A/C with LN susceptibility. METHODS: The study was...

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Autores principales: Abdallah, Emad, Waked, Emam, Abdelwahab, Mahmoud A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4811976/
https://www.ncbi.nlm.nih.gov/pubmed/27069855
http://dx.doi.org/10.1016/j.krcp.2015.11.002
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author Abdallah, Emad
Waked, Emam
Abdelwahab, Mahmoud A.
author_facet Abdallah, Emad
Waked, Emam
Abdelwahab, Mahmoud A.
author_sort Abdallah, Emad
collection PubMed
description BACKGROUND: Interleukin-10 (IL-10) is an important immunoregulatory cytokine. There are few studies evaluating the association between IL-10 and lupus nephritis (LN). The aim of this study was to evaluate the association of IL-10 gene promoter -592 A/C with LN susceptibility. METHODS: The study was conducted on 84 patients with systemic lupus erythematosus (SLE). Patients were divided into LN group (Group I, 48 patients) and non-LN group (Group II, 36 patients). The -592 A/C polymorphisms in IL-10 promoter gene were determined by polymerase chain reaction and restriction fragment length polymorphism in both groups. IL-10 was determined by enzyme-linked immunosorbent assay. Frequencies of the genotypes were compared between LN and non-LN patients and among LN patients with different pathologic classes. RESULTS: There was a significant increase in serum level of IL-10 (P = 0.001) in Group I compared with Group II and significant positive correlation between serum IL-10 and SLE disease activity index (r = 0.466, P = 0.001) in Group I. There were no significant differences in the distribution of the IL-10 gene promoter -592 A/C genotypes or the allele frequencies between Groups I and II. There was no significant difference between AC/CC and AA genotypes with SLE disease activity index, proteinuria, hematuria, anti-double-stranded DNA, and IL-10 in Group I. There was no significant difference in the distribution of AC and CC genotypes among different pathologic LN classes. CONCLUSION: IL-10 suggested to play a role in pathogenesis and development of LN. However, the promoter -592 A/C of IL-10 gene suggested to be not associated with serum IL-10 levels or LN susceptibility. In addition, it appears that promoter -592 A/C of IL-10 gene not associated with LN activity or the pathologic classes of LN.
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spelling pubmed-48119762016-04-11 Evaluating the association of interleukin-10 gene promoter -592 A/C polymorphism with lupus nephritis susceptibility Abdallah, Emad Waked, Emam Abdelwahab, Mahmoud A. Kidney Res Clin Pract Original Article BACKGROUND: Interleukin-10 (IL-10) is an important immunoregulatory cytokine. There are few studies evaluating the association between IL-10 and lupus nephritis (LN). The aim of this study was to evaluate the association of IL-10 gene promoter -592 A/C with LN susceptibility. METHODS: The study was conducted on 84 patients with systemic lupus erythematosus (SLE). Patients were divided into LN group (Group I, 48 patients) and non-LN group (Group II, 36 patients). The -592 A/C polymorphisms in IL-10 promoter gene were determined by polymerase chain reaction and restriction fragment length polymorphism in both groups. IL-10 was determined by enzyme-linked immunosorbent assay. Frequencies of the genotypes were compared between LN and non-LN patients and among LN patients with different pathologic classes. RESULTS: There was a significant increase in serum level of IL-10 (P = 0.001) in Group I compared with Group II and significant positive correlation between serum IL-10 and SLE disease activity index (r = 0.466, P = 0.001) in Group I. There were no significant differences in the distribution of the IL-10 gene promoter -592 A/C genotypes or the allele frequencies between Groups I and II. There was no significant difference between AC/CC and AA genotypes with SLE disease activity index, proteinuria, hematuria, anti-double-stranded DNA, and IL-10 in Group I. There was no significant difference in the distribution of AC and CC genotypes among different pathologic LN classes. CONCLUSION: IL-10 suggested to play a role in pathogenesis and development of LN. However, the promoter -592 A/C of IL-10 gene suggested to be not associated with serum IL-10 levels or LN susceptibility. In addition, it appears that promoter -592 A/C of IL-10 gene not associated with LN activity or the pathologic classes of LN. Elsevier 2016-03 2015-12-02 /pmc/articles/PMC4811976/ /pubmed/27069855 http://dx.doi.org/10.1016/j.krcp.2015.11.002 Text en Copyright © 2016. The Korean Society of Nephrology. Published by Elsevier. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Original Article
Abdallah, Emad
Waked, Emam
Abdelwahab, Mahmoud A.
Evaluating the association of interleukin-10 gene promoter -592 A/C polymorphism with lupus nephritis susceptibility
title Evaluating the association of interleukin-10 gene promoter -592 A/C polymorphism with lupus nephritis susceptibility
title_full Evaluating the association of interleukin-10 gene promoter -592 A/C polymorphism with lupus nephritis susceptibility
title_fullStr Evaluating the association of interleukin-10 gene promoter -592 A/C polymorphism with lupus nephritis susceptibility
title_full_unstemmed Evaluating the association of interleukin-10 gene promoter -592 A/C polymorphism with lupus nephritis susceptibility
title_short Evaluating the association of interleukin-10 gene promoter -592 A/C polymorphism with lupus nephritis susceptibility
title_sort evaluating the association of interleukin-10 gene promoter -592 a/c polymorphism with lupus nephritis susceptibility
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4811976/
https://www.ncbi.nlm.nih.gov/pubmed/27069855
http://dx.doi.org/10.1016/j.krcp.2015.11.002
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