Risk Association Between the NF-κB1 -94ins/delATTG Promoter Polymorphism and Inflammatory Bowel Diseases: A Meta-Analysis
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Extensive investigation of the NF-κB1 -94ins/delATTG promoter polymorphism for risk association with ulcerative colitis (UC) and Crohn’s disease (CD) risk has yielded conflicting results.
The objective of this meta-analysis was to evaluate the risk association between the NF-κB1 -94ins/delATTG promoter polymorphism and UC and CD.
All eligible case–control studies of the association of NF-κB1 -94ins/delATTG promoter polymorphism with UC and CD were identified in the Pubmed and Embase databases. From these data, odds ratios (OR) with 95 % confidence intervals (CI) were calculated. Meta-analysis was performed for alleles (D vs. W) and genotypes (DD + WD vs. WW, DD vs. WW + WD, DD vs. WW, WD vs. WW) in a fixed/random effects model.
Nine case–control studies that included 4,447 cases (2,631 UC and 1,816 CD) and 2,195 controls were identified. Results indicated increased risk association of D allele carriers with UC (D vs. W: OR = 1.08, 95 % CI = 1.01–1.17, P = 0.03; DD vs. WW + WD: OR = 1.16, 95 % CI = 1.01–1.32, P = 0.04 and DD vs. WW: OR = 1.20, 95 % CI = 1.03–1.39, P = 0.02). No risk association was identified with CD.
This meta-analysis indicated that the NF-κB1 -94ins/delATTG promoter polymorphism is a risk factor for UC but not CD.
- Bonen DK, Cho JH. The genetics of inflammatory bowel disease. Gastroenterology. 2003;124:524–536.
- De Vry CG, Prasad S, Komuves L, et al. Non-viral delivery of nuclear factor-kappaB decoy ameliorates murine inflammatory bowel disease and restores tissue homeostasis. Gut. 2007;56:524–533. CrossRef
- Takedatsu H, Taylor KD, Mei L, et al. Linkage of Crohn’s disease-related serological phenotypes: NF-κB1 haplotypes are associated with anti-CBir1 and ASCA, and show reduced NF-kappaB activation. Gut. 2009;58:60–67. CrossRef
- Le Beau MM, Ito C, Cogswell P, Espinosa R 3rd, Fernald AA, Baldwin AS Jr. Chromosomal localization of the genes encoding the p50/p105 subunits of NF-kappa B (NF-κB2) and the I kappa B/MAD-3 (NF-κBI) inhibitor of NF-kappa B to 4q24 and 14q13, respectively. Genomics. 1992;14:529–531. CrossRef
- Mathew S, Murty VV, Dalla-Favera R, Chaganti RS. Chromosomal localization of genes encoding the transcription factors, c-rel, NF-kappa Bp50, NF-kappa Bp65, and lyt-10 by fluorescence in situ hybridization. Oncogene. 1993;8:191–193.
- Beinke S, Ley SC. Functions of NF-kappaB1 and NF-kappaB2 in immune cell biology. Biochem J. 2004;382:393–409. CrossRef
- Karban AS, Okazaki T, Panhuysen CI, et al. Functional annotation of a novel NF-κB1 promoter polymorphism that increases risk for ulcerative colitis. Hum Mol Genet. 2004;13:35–45. CrossRef
- Borm ME, van Bodegraven AA, Mulder CJ, Kraal G, Bouma G. A NF-κB1 promoter polymorphism is involved in susceptibility to ulcerative colitis. Int J Immunogenet. 2005;32:401–405. CrossRef
- Oliver J, Gómez-García M, Paco L, et al. A functional polymorphism of the NF-κB1 promoter is not associated with ulcerative colitis in a Spanish population. Inflamm Bowel Dis. 2005;11:576–579. CrossRef
- Mirza MM, Fisher SA, Onnie C, et al. No association of the NF-κB1 promoter polymorphism with ulcerative colitis in a British case control cohort. Gut. 2005;54:1205–1206. CrossRef
- Glas J, Török HP, Tonenchi L, et al. Role of the NF-κB1-94ins/delATTG promoter polymorphism in IBD and potential interactions with polymorphisms in the CARD15/NOD2, IKBL, and IL-1RN genes. Inflamm Bowel Dis. 2006;12:606–611. CrossRef
- Latiano A, Palmieri O, Valvano MR, et al. Evaluating the role of the genetic variations of PTPN22, NF-κB1, and FcGRIIIA genes in inflammatory bowel disease: a meta-analysis. Inflamm Bowel Dis. 2007;13:1212–1219. CrossRef
- Szamosi T, Lakatos PL, Hungarian IBD Study Group, et al. The 3′UTR NF-κBIA variant is associated with extensive colitis in Hungarian IBD patients. Dig Dis Sci. 2009;54:351–359. CrossRef
- Lei Y, Deng C-S. Association of NF-κB1 -94ins/delATTG promoter polymorphism with ulcerative colitis in Chinese Han population of Hubei Province. World Chin J Digestol. 2009;17:2212–2216.
- Andersen V, Christensen J, Ernst A, et al. Polymorphisms in NF-κB, PXR, LXR, PPARγ and risk of inflammatory bowel disease. World J Gastroenterol. 2011;17:197–206. CrossRef
- Zou YF, Wang F, Feng XL, et al. Association of NF-κB1 -94ins/delATTG promoter polymorphism with susceptibility to autoimmune and inflammatory diseases: a meta-analysis. Tissue Antigens. 2011;77:9–17. CrossRef
- Zou YF, Yuan FL, Feng XL, et al. Association between NF-κB1 -94ins/delATTG promoter polymorphism and cancer risk: a meta-analysis. Cancer Invest. 2011;29:78–85. CrossRef
- Andersen V, Christensen J, Østergaard M et al. Association of the nuclear receptors PXR, LXR and PPARγ with ulcerative colitis in the Danish population: a case-control study. Inflamm Bowel Dis. 2009;15:S29.
- Borm ME, He J, Kelsall B, Peña AS, Strober W, Bouma G. A major quantitative trait locus on mouse chromosome 3 is involved in disease susceptibility in different colitis models. Gastroenterology. 2005;128:74–85. CrossRef
- Farmer MA, Sundberg JP, Bristol IJ, et al. A major quantitative trait locus on chromosome 3 controls colitis severity in IL-10-deficient mice. Proc Natl Acad Sci USA. 2001;98:13820–13825. CrossRef
- Chang M, Lee AJ, Fitzpatrick L, Zhang M, Sun SC. NF-kappaB1 p105 regulates T cell homeostasis and prevents chronic inflammation. J Immunol. 2009;182:3131–3138. CrossRef
- Tomczak MF, Erdman SE, Poutahidis T, et al. NF-kappa B is required within the innate immune system to inhibit microflora-induced colitis and expression of IL-12 p40. J Immunol. 2003;171:1484–1492.
- Hampe J, Schreiber S, Shaw SH, et al. A genomewide analysis provides evidence for novel linkages in inflammatory bowel disease in a large European cohort. Am J Hum Genet. 1999;64:808–816. CrossRef
- Cho JH, Nicolae DL, Gold LH, et al. Identification of novel susceptibility loci for inflammatory bowel disease on chromosomes 1p, 3q, and 4q: evidence for epistasis between 1p and IBD1. Proc Natl Acad Sci USA. 1998;95:7502–7507. CrossRef
- Atreya I, Atreya R, Neurath MF. NF-kappaB in inflammatory bowel disease. J Intern Med. 2008;263:591–596. CrossRef
- Ishikawa H, Claudio E, Dambach D, Raventós-Suárez C, Ryan C, Bravo R. Chronic inflammation and susceptibility to bacterial infections in mice lacking the polypeptide (p)105 precursor (NF-κB1) but expressing p50. J Exp Med. 1998;187:985–996. CrossRef
- Erdman S, Fox JG, Dangler CA, Feldman D, Horwitz BH. Typhlocolitis in NF-kappa B-deficient mice. J Immunol. 2001;166:1443–1447.
- Baer M, Dillner A, Schwartz RC, Sedon C, Nedospasov S, Johnson PF. Tumor necrosis factor alpha transcription in macrophages is attenuated by an autocrine factor that preferentially induces NF-kappaB p50. Mol Cell Biol. 1998;18:5678–5689.
- Visekruna A, Joeris T, Seidel D, et al. Proteasome-mediated degradation of IkappaBalpha and processing of p105 in Crohn disease and ulcerative colitis. J Clin Invest. 2006;116:3195–3203. CrossRef
- Driessler F, Venstrom K, Sabat R, Asadullah K, Schottelius AJ. Molecular mechanisms of interleukin-10-mediated inhibition of NF-kappaB activity: a role for p50. Clin Exp Immunol. 2004;135:64–73. CrossRef
- Tomczak MF, Erdman SE, Davidson A, et al. Inhibition of Helicobacter hepaticus-induced colitis by IL-10 requires the p50/p105 subunit of NF-kappa B. J Immunol. 2006;177:7332–7339.
- Risk Association Between the NF-κB1 -94ins/delATTG Promoter Polymorphism and Inflammatory Bowel Diseases: A Meta-Analysis
Digestive Diseases and Sciences
Volume 57, Issue 9 , pp 2304-2309
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