Macrophage migration inhibitory factor gene polymorphisms in inflammatory bowel disease: An association study in New Zealand Caucasians and meta-analysis

作者：Falvey James D; Bentley Robert W; Merriman Tony R; Hampton Mark B; Barclay Murray L; Gearry Richard B; Roberts Rebecca L^*

来源：World Journal of Gastroenterology, 2013, 19(39): 6656-6664.

DOI：10.3748/wjg.v19.i39.6656

AIM: To investigate the association of macrophage migration inhibitory factor (MIF) promoter polymorphisms with inflammatory bowel disease (IBD) risk. %26lt;br%26gt;METHODS: One thousand and six New Zealand Caucasian cases and 540 Caucasian controls were genotyped for the MIF SNP -173G %26gt; C (rs755622) and the repeat polymorphism CATT5-8 (rs5844572) using a predesigned TaqMan SNP assay and capillary electrophoresis, respectively. Data were analysed for single site and haplotype association with IBD risk and phenotype. Meta-analysis was employed, to assess cumulative evidence of association of MIF-173G %26gt; C with IBD. All published genotype data for MIF -173G %26gt; C in IBD were identified using PubMed and subsequently searching the references of all PubMed-identified studies. Imputed genotypes for MIF-173G %26gt; C were generated from the Wellcome Trust Case Control Consortium (and National Institute of Diabetes and Digestive and Kidney Diseases). Separate meta-analyses were performed on Caucasian Crohn%26apos;s disease (CD) (3863 patients, 6031 controls), Caucasian ulcerative colitis (UC) (1260 patients, 1987 controls), and East Asian UC (416 patients and 789 controls) datasets using the Mantel-Haenszel method. The New Zealand dataset had 93% power, and the meta-analyses had 100% power to detect an effect size of OR = 1.40 at a = 0.05, respectively. %26lt;br%26gt;RESULTS: In our New Zealand dataset, single-site analysis found no evidence of association of MIF polymorphisms with overall risk of CD, UC, and IBD or disease phenotype (all P values %26gt; 0.05). Haplotype analysis found the CATT5/-173C haplotype occurred at a higher frequency in New Zealand controls compared to IBD patients (0.6 vs 0.01; P = 0.03, OR = 0.22; 95% CI: 0.05-0.99), but this association did not survive bonferroni correction. Meta-analysis of our New Zealand MIF-173G %26gt; C data with data from seven additional Caucasian datasets using a random effects model found no association of MIF polymorphisms with CD, UC, or overall IBD. Similarly, meta-analysis of all published MIF-173G %26gt; C data from East Asian datasets (416 UC patients, 789 controls) found no association of this promoter polymorphism with UC. %26lt;br%26gt;CONCLUSION: We found no evidence of association of MIF promoter polymorphisms with IBD.

• 出版日期2013-10-21