The cannabinoid 1 receptor (CNR1) 1359 G/A polymorphism modulates susceptibility to ulcerative colitis and the phenotype in Crohn's disease.

<h4>Background</h4>Recent evidence suggests a crucial role of the endocannabinoid system, including the cannabinoid 1 receptor (CNR1), in intestinal inflammation. We therefore investigated the influence of the CNR1 1359 G/A (p.Thr453Thr; rs1049353) single nucleotide polymorphism (SNP) on...

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Autores principales: Martin Storr, Dominik Emmerdinger, Julia Diegelmann, Simone Pfennig, Thomas Ochsenkühn, Burkhard Göke, Peter Lohse, Stephan Brand
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Publicado: Public Library of Science (PLoS) 2010
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spelling oai:doaj.org-article:da13048bf34d4a2d8f8e486e7f896ad62021-11-25T06:25:31ZThe cannabinoid 1 receptor (CNR1) 1359 G/A polymorphism modulates susceptibility to ulcerative colitis and the phenotype in Crohn's disease.1932-620310.1371/journal.pone.0009453https://doaj.org/article/da13048bf34d4a2d8f8e486e7f896ad62010-02-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20195480/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Recent evidence suggests a crucial role of the endocannabinoid system, including the cannabinoid 1 receptor (CNR1), in intestinal inflammation. We therefore investigated the influence of the CNR1 1359 G/A (p.Thr453Thr; rs1049353) single nucleotide polymorphism (SNP) on disease susceptibility and phenotype in patients with ulcerative colitis (UC) and Crohn's disease (CD).<h4>Methods</h4>Genomic DNA from 579 phenotypically well-characterized individuals was analyzed for the CNR1 1359 G/A SNP. Amongst these were 166 patients with UC, 216 patients with CD, and 197 healthy controls.<h4>Results</h4>Compared to healthy controls, subjects A/A homozygous for the CNR1 1359 G/A SNP had a reduced risk to develop UC (p = 0.01, OR 0.30, 95% CI 0.12-0.78). The polymorphism did not modulate CD susceptibility, but carriers of the minor A allele had a lower body mass index than G/G wildtype carriers (p = 0.0005). In addition, homozygous carriers of the G allele were more likely to develop CD before 40 years of age (p = 5.9x10(-7)) than carriers of the A allele.<h4>Conclusion</h4>The CNR1 p.Thr453Thr polymorphism appears to modulate UC susceptibility and the CD phenotype. The endocannabinoid system may influence the manifestation of inflammatory bowel diseases, suggesting endocannabinoids as potential target for future therapies.Martin StorrDominik EmmerdingerJulia DiegelmannSimone PfennigThomas OchsenkühnBurkhard GökePeter LohseStephan BrandPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 5, Iss 2, p e9453 (2010)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Martin Storr
Dominik Emmerdinger
Julia Diegelmann
Simone Pfennig
Thomas Ochsenkühn
Burkhard Göke
Peter Lohse
Stephan Brand
The cannabinoid 1 receptor (CNR1) 1359 G/A polymorphism modulates susceptibility to ulcerative colitis and the phenotype in Crohn's disease.
description <h4>Background</h4>Recent evidence suggests a crucial role of the endocannabinoid system, including the cannabinoid 1 receptor (CNR1), in intestinal inflammation. We therefore investigated the influence of the CNR1 1359 G/A (p.Thr453Thr; rs1049353) single nucleotide polymorphism (SNP) on disease susceptibility and phenotype in patients with ulcerative colitis (UC) and Crohn's disease (CD).<h4>Methods</h4>Genomic DNA from 579 phenotypically well-characterized individuals was analyzed for the CNR1 1359 G/A SNP. Amongst these were 166 patients with UC, 216 patients with CD, and 197 healthy controls.<h4>Results</h4>Compared to healthy controls, subjects A/A homozygous for the CNR1 1359 G/A SNP had a reduced risk to develop UC (p = 0.01, OR 0.30, 95% CI 0.12-0.78). The polymorphism did not modulate CD susceptibility, but carriers of the minor A allele had a lower body mass index than G/G wildtype carriers (p = 0.0005). In addition, homozygous carriers of the G allele were more likely to develop CD before 40 years of age (p = 5.9x10(-7)) than carriers of the A allele.<h4>Conclusion</h4>The CNR1 p.Thr453Thr polymorphism appears to modulate UC susceptibility and the CD phenotype. The endocannabinoid system may influence the manifestation of inflammatory bowel diseases, suggesting endocannabinoids as potential target for future therapies.
format article
author Martin Storr
Dominik Emmerdinger
Julia Diegelmann
Simone Pfennig
Thomas Ochsenkühn
Burkhard Göke
Peter Lohse
Stephan Brand
author_facet Martin Storr
Dominik Emmerdinger
Julia Diegelmann
Simone Pfennig
Thomas Ochsenkühn
Burkhard Göke
Peter Lohse
Stephan Brand
author_sort Martin Storr
title The cannabinoid 1 receptor (CNR1) 1359 G/A polymorphism modulates susceptibility to ulcerative colitis and the phenotype in Crohn's disease.
title_short The cannabinoid 1 receptor (CNR1) 1359 G/A polymorphism modulates susceptibility to ulcerative colitis and the phenotype in Crohn's disease.
title_full The cannabinoid 1 receptor (CNR1) 1359 G/A polymorphism modulates susceptibility to ulcerative colitis and the phenotype in Crohn's disease.
title_fullStr The cannabinoid 1 receptor (CNR1) 1359 G/A polymorphism modulates susceptibility to ulcerative colitis and the phenotype in Crohn's disease.
title_full_unstemmed The cannabinoid 1 receptor (CNR1) 1359 G/A polymorphism modulates susceptibility to ulcerative colitis and the phenotype in Crohn's disease.
title_sort cannabinoid 1 receptor (cnr1) 1359 g/a polymorphism modulates susceptibility to ulcerative colitis and the phenotype in crohn's disease.
publisher Public Library of Science (PLoS)
publishDate 2010
url https://doaj.org/article/da13048bf34d4a2d8f8e486e7f896ad6
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