Top

Digestive Diseases and Sciences

Published in:

01-09-2012 | Original Article

Risk Association Between the NF-κB1 -94ins/delATTG Promoter Polymorphism and Inflammatory Bowel Diseases: A Meta-Analysis

Authors: Meilan Liang, Xinyu Xu, Yaoyao Gong, Yurong Tang, Lin Lin

Published in: Digestive Diseases and Sciences | Issue 9/2012

Abstract

Background

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.

Aims

The objective of this meta-analysis was to evaluate the risk association between the NF-κB1 -94ins/delATTG promoter polymorphism and UC and CD.

Methods

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.

Results

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.

Conclusion

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.PubMedCrossRef

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.PubMedCrossRef

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.PubMedCrossRef

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.PubMed

Beinke S, Ley SC. Functions of NF-kappaB1 and NF-kappaB2 in immune cell biology. Biochem J. 2004;382:393–409.PubMedCrossRef

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.PubMedCrossRef

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.PubMedCrossRef

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.PubMedCrossRef

10.

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.PubMedCrossRef

11.

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.PubMedCrossRef

12.

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.PubMedCrossRef

13.

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.PubMedCrossRef

14.

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.

15.

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.PubMedCrossRef

16.

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.PubMedCrossRef

17.

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.PubMedCrossRef

18.

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.

19.

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.PubMedCrossRef

20.

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.PubMedCrossRef

21.

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.PubMedCrossRef

22.

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.PubMed

23.

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.PubMedCrossRef

24.

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.PubMedCrossRef

25.

Atreya I, Atreya R, Neurath MF. NF-kappaB in inflammatory bowel disease. J Intern Med. 2008;263:591–596.PubMedCrossRef

26.

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.PubMedCrossRef

27.

Erdman S, Fox JG, Dangler CA, Feldman D, Horwitz BH. Typhlocolitis in NF-kappa B-deficient mice. J Immunol. 2001;166:1443–1447.PubMed

28.

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.PubMed

29.

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.PubMedCrossRef

30.

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.PubMedCrossRef

31.

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.PubMed

Title: Risk Association Between the NF-κB1 -94ins/delATTG Promoter Polymorphism and Inflammatory Bowel Diseases: A Meta-Analysis
Authors: Meilan Liang
Xinyu Xu
Yaoyao Gong
Yurong Tang
Lin Lin
Publication date: 01-09-2012
Publisher: Springer US
Published in: Digestive Diseases and Sciences / Issue 9/2012
Print ISSN: 0163-2116
Electronic ISSN: 1573-2568
DOI: https://doi.org/10.1007/s10620-012-2164-x

Live Webinar | 27-06-2024 | 18:00 (CEST)

Keynote webinar | Spotlight on medication adherence

Reserve your place

Live: Thursday 27th June 2024, 18:00-19:30 (CEST)

WHO estimates that half of all patients worldwide are non-adherent to their prescribed medication. The consequences of poor adherence can be catastrophic, on both the individual and population level.

Join our expert panel to discover why you need to understand the drivers of non-adherence in your patients, and how you can optimize medication adherence in your clinics to drastically improve patient outcomes.

Prof. Kevin Dolgin

Prof. Florian Limbourg

Prof. Anoop Chauhan

Developed by: Springer Medicine

Obesity Clinical Trial Summary

At a glance: The STEP trials

A round-up of the STEP phase 3 clinical trials evaluating semaglutide for weight loss in people with overweight or obesity.

Developed by: Springer Medicine

Keynote webinar | Spotlight on medication adherence

Springer Medicine

Abstract

Background

Aims

Methods

Results

Conclusion

Please log in to get access to this content

Other articles of this Issue 9/2012

Autoimmune Pancreatitis (AIP) Masquerading as Pancreatic Cancer: Cutting Is Not a Crime … for Now

Predictors of Early Stent Occlusion Among Plastic Biliary Stents

Moxibustion Inhibits Apoptosis and Tumor Necrosis Factor-Alpha/Tumor Necrosis Factor Receptor 1 in the Colonic Epithelium of Crohn’s Disease Model Rats

Coated Transjugular Intrahepatic Portosystemic Shunt Does Not Improve Thrombocytopenia in Patients with Liver Cirrhosis

Proton Pump Inhibitors Increase the Incidence of Bone Fractures in Hepatitis C Patients

Expression of Toll-Like Receptors in Enterocromaffin-Like Cells and Their Function in Histamine Release

Keynote webinar | Spotlight on medication adherence

Live: Thursday 27th June 2024, 18:00-19:30 (CEST)

At a glance: The STEP trials