Clinical Research
Copyright ©2008 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. Aug 7, 2008; 14(29): 4652-4661
Published online Aug 7, 2008. doi: 10.3748/wjg.14.4652
Single nucleotide polymorphism in the tumor necrosis factor-alpha gene affects inflammatory bowel diseases risk
Lynnette R Ferguson, Claudia Huebner, Ivonne Petermann, Richard B Gearry, Murray L Barclay, Pieter Demmers, Alan McCulloch, Dug Yeo Han
Lynnette R Ferguson, Claudia Huebner, Ivonne Petermann, Dug Yeo Han, Discipline of Nutrition, the University of Auckland, Private Bag 92019, Auckland 1142, New Zealand
Richard B Gearry, Murray L Barclay, Department of Gastroenterology, Christchurch Hospital, Christchurch 8140, New Zealand
Pieter Demmers, Crop and Food Research, Mosgiel 9053, New Zealand
Alan McCulloch, AgResearch Limited, Mosgiel 9053, New Zealand
Author contributions: Ferguson LR, Huebner C and Petermann I designed research; Huebner C and Petermann I performed research; Gearry RB and Barclay ML contributed human subjects and DNA samples, Demmers P and McCulloch A contributed analytic tools; Han DY analyzed data; and Ferguson LR wrote the paper.
Correspondence to: Lynnette R Ferguson, Professor, Discipline of Nutrition, the University of Auckland, Private Bag 92019, Auckland, New Zealand. l.ferguson@auckland.ac.nz
Telephone: +64-9-3737599-86372
Fax: +64-9-3035962
Received: May 8, 2008
Revised: June 30, 2008
Accepted: July 7, 2008
Published online: August 7, 2008
Abstract

AIM: To investigate the role that single nucleotide polymorphisms (SNPs) in the promoter of the tumour necrosis factor-alpha (TNF-α) gene play in the risk of inflammatory bowel diseases (IBDs) in a New Zealand population, in the context of international studies.

METHODS: DNA samples from 388 patients with Crohn’s disease (CD), 405 ulcerative colitis (UC), 27 indeterminate colitis (IC) and 201 randomly selected controls, from Canterbury, New Zealand were screened for 3 common polymorphisms in the TNF-α receptor: -238 G→A, -308 G→A and -857C→T, using a TaqmanR assay. A meta-analysis was performed on the data obtained on these polymorphisms combined with that from other published studies.

RESULTS: Individuals carrying the -308 G/A allele had a significantly (OR = 1.91, χ2 = 17.36, P < 0.0001) increased risk of pancolitis, and a 1.57-fold increased risk (OR = 1.57, χ2 = 4.34, P = 0.037) of requiring a bowel resection in UC. Carrying the -857 C/T variant decreased the risk of ileocolonic CD (OR = 0.56, χ2 = 4.32, P = 0.037), and the need for a bowel resection (OR = 0.59, χ2 = 4.85, P = 0.028). The risk of UC was reduced in individuals who were smokers at diagnosis, (OR = 0.48, χ2 = 4.86, P = 0.028).

CONCLUSION: TNF-α is a key cytokine known to play a role in inflammatory response, and the locus for the gene is found in the IBD3 region on chromosome 6p21, known to be associated with an increased risk for IBD. The -308 G/A SNP in the TNF-α promoter is functional, and may account in part for the increased UC risk associated with the IBD3 genomic region. The -857 C/T SNP may decrease IBD risk in certain groups. Pharmaco- or nutrigenomic approaches may be desirable for individuals with such affected genotypes.

Keywords: Tumour necrosis factor alpha; Single nucleotide polymorphisms; Inflammatory bowel diseases; Crohn’s disease; Ulcerative colitis