The functional -765G→C polymorphism of the COX-2 gene may reduce the risk of developing crohn's disease.
<h4>Background</h4>Cyclooxygenase-2 (COX-2) is a key enzyme involved in the conversion of arachidonic acid into prostaglandins. COX-2 is mainly induced at sites of inflammation in response to proinflammatory cytokines such as interleukin-1α/β, interferon-γ and tumor necrosis factor-α pro...
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oai:doaj.org-article:70f4f6a05b2f4637b3efa9d081aae6342021-11-18T07:36:35ZThe functional -765G→C polymorphism of the COX-2 gene may reduce the risk of developing crohn's disease.1932-620310.1371/journal.pone.0015011https://doaj.org/article/70f4f6a05b2f4637b3efa9d081aae6342010-11-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21124790/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Cyclooxygenase-2 (COX-2) is a key enzyme involved in the conversion of arachidonic acid into prostaglandins. COX-2 is mainly induced at sites of inflammation in response to proinflammatory cytokines such as interleukin-1α/β, interferon-γ and tumor necrosis factor-α produced by inflammatory cells.<h4>Aim</h4>The aim of this study was to investigate the possible modulating effect of the functional COX-2 polymorphisms -1195 A→G and -765G→C on the risk for development of inflammatory bowel disease (IBD) in a Dutch population.<h4>Methods</h4>Genomic DNA of 525 patients with Crohn's disease (CD), 211 patients with ulcerative colitis (UC) and 973 healthy controls was genotyped for the -1195 A→G (rs689466) and -765G→C (rs20417) polymorphisms. Distribution of genotypes in patients and controls were compared and genotype-phenotype interactions were investigated.<h4>Results</h4>The genotype distribution of the -1195A→G polymorphism was not different between the patients with CD or UC and the control group. The -765GG genotype was more prevalent in CD patients compared to controls with an OR of 1.33 (95%CI 1.04-1.69, p<0.05). The -765GC and -765CC genotype carriers showed a tendency to be less frequent in patients with CD compared to controls, with ORs of 0.78 (95%CI: 0.61-1.00) and 0.49 (95%CI 0.22-1.08), respectively. Combining homozygous and heterozygous patients with the -765C allele showed a reduced risk for developing CD, with an OR of 0.75 (95%CI: 0.59-0.96). In the context of this, the G(-1195)G(-765)/A(-1195)C(-765) diplotype was significantly less common in patients with CD compared to controls, with an OR of 0.62 (95%CI: 0.39-0.98). For UC however, such an effect was not observed. No correlation was found between COX-2 diplotypes and clinical characteristics of IBD.<h4>Conclusions</h4>The -765G→C polymorphism was associated with a reduced risk for developing Crohn's disease in a Dutch population.Hilbert S de VriesRene H M te MorscheMartijn G H van OijenIris D NagtegaalWilbert H M PetersDirk J de JongPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 5, Iss 11, p e15011 (2010) |
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Medicine R Science Q Hilbert S de Vries Rene H M te Morsche Martijn G H van Oijen Iris D Nagtegaal Wilbert H M Peters Dirk J de Jong The functional -765G→C polymorphism of the COX-2 gene may reduce the risk of developing crohn's disease. |
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<h4>Background</h4>Cyclooxygenase-2 (COX-2) is a key enzyme involved in the conversion of arachidonic acid into prostaglandins. COX-2 is mainly induced at sites of inflammation in response to proinflammatory cytokines such as interleukin-1α/β, interferon-γ and tumor necrosis factor-α produced by inflammatory cells.<h4>Aim</h4>The aim of this study was to investigate the possible modulating effect of the functional COX-2 polymorphisms -1195 A→G and -765G→C on the risk for development of inflammatory bowel disease (IBD) in a Dutch population.<h4>Methods</h4>Genomic DNA of 525 patients with Crohn's disease (CD), 211 patients with ulcerative colitis (UC) and 973 healthy controls was genotyped for the -1195 A→G (rs689466) and -765G→C (rs20417) polymorphisms. Distribution of genotypes in patients and controls were compared and genotype-phenotype interactions were investigated.<h4>Results</h4>The genotype distribution of the -1195A→G polymorphism was not different between the patients with CD or UC and the control group. The -765GG genotype was more prevalent in CD patients compared to controls with an OR of 1.33 (95%CI 1.04-1.69, p<0.05). The -765GC and -765CC genotype carriers showed a tendency to be less frequent in patients with CD compared to controls, with ORs of 0.78 (95%CI: 0.61-1.00) and 0.49 (95%CI 0.22-1.08), respectively. Combining homozygous and heterozygous patients with the -765C allele showed a reduced risk for developing CD, with an OR of 0.75 (95%CI: 0.59-0.96). In the context of this, the G(-1195)G(-765)/A(-1195)C(-765) diplotype was significantly less common in patients with CD compared to controls, with an OR of 0.62 (95%CI: 0.39-0.98). For UC however, such an effect was not observed. No correlation was found between COX-2 diplotypes and clinical characteristics of IBD.<h4>Conclusions</h4>The -765G→C polymorphism was associated with a reduced risk for developing Crohn's disease in a Dutch population. |
format |
article |
author |
Hilbert S de Vries Rene H M te Morsche Martijn G H van Oijen Iris D Nagtegaal Wilbert H M Peters Dirk J de Jong |
author_facet |
Hilbert S de Vries Rene H M te Morsche Martijn G H van Oijen Iris D Nagtegaal Wilbert H M Peters Dirk J de Jong |
author_sort |
Hilbert S de Vries |
title |
The functional -765G→C polymorphism of the COX-2 gene may reduce the risk of developing crohn's disease. |
title_short |
The functional -765G→C polymorphism of the COX-2 gene may reduce the risk of developing crohn's disease. |
title_full |
The functional -765G→C polymorphism of the COX-2 gene may reduce the risk of developing crohn's disease. |
title_fullStr |
The functional -765G→C polymorphism of the COX-2 gene may reduce the risk of developing crohn's disease. |
title_full_unstemmed |
The functional -765G→C polymorphism of the COX-2 gene may reduce the risk of developing crohn's disease. |
title_sort |
functional -765g→c polymorphism of the cox-2 gene may reduce the risk of developing crohn's disease. |
publisher |
Public Library of Science (PLoS) |
publishDate |
2010 |
url |
https://doaj.org/article/70f4f6a05b2f4637b3efa9d081aae634 |
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