Dataset Information

TNF-? -308 G?>?A (rs1800629) Polymorphism is Associated with Celiac Disease: A Meta-analysis of 11 Case-Control Studies.

ABSTRACT: Celiac disease (CD) remains one of the most significant autoimmune diseases worldwide. The pathogenesis of CD is not clearly understood and is probably attributed to genomic variations and host genetic make-up. Case-control and cohort studies of the association between the TNF-? -308 G?>?A (rs1800629) polymorphism and CD susceptibility have yielded inconsistent results. In this study, PubMed, EMBASE, and Google Scholar web-databases were searched for pertinent reports showing association of TNF-? -308 G?>?A gene with CD risk. A total of eleven reports involving 1774 controls and 1147 CD cases were included. Significant associations in four genetic models, viz. variant allele (A vs. G: p?=?0.001; OR?=?2.051, 95% CI?=?1.452-2.895), variant homozygous (AA vs. GG: p?=?0.001; OR?=?6.626, 95% CI?=?3.569-12.300), recessive (AA vs. GG?+?AG: p?=?0.001; OR?=?4.766, 95% CI?=?3.177-7.152) and dominant (AA?+?AG vs. GG: p?=?0.008; OR?=?1.910, 95% CI?=?1.181-3.088) were found in comparison with wild type homozygous GG genotype. However, heterozygous genetic model did not show any association. Sensitivity analysis revealed stable and statistically robust results. Our results suggest that TNF-? -308 G?>?A gene polymorphism significantly contributes to CD susceptibility.

SUBMITTER: Khan S

PROVIDER: S-EPMC5011702 | biostudies-literature | 2016 Sep

REPOSITORIES: biostudies-literature

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TNF-α -308 G > A (rs1800629) Polymorphism is Associated with Celiac Disease: A Meta-analysis of 11 Case-Control Studies.

Khan Saif S Khan Saif S Mandal Raju K RK Jawed Arshad A Dar Sajad A SA Wahid Mohd M Panda Aditya K AK Areeshi Mohammed Y MY Ahmed Khan Md Ekhlaque ME Haque Shafiul S

Scientific reports 20160906

Celiac disease (CD) remains one of the most significant autoimmune diseases worldwide. The pathogenesis of CD is not clearly understood and is probably attributed to genomic variations and host genetic make-up. Case-control and cohort studies of the association between the TNF-α -308 G > A (rs1800629) polymorphism and CD susceptibility have yielded inconsistent results. In this study, PubMed, EMBASE, and Google Scholar web-databases were searched for pertinent reports showing association of TNF- ...[more]

PMID: 27597177

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Project description:BackgroundAngina pectoris (AP) occurs when oxygen and other nutrients are insufficient to meet the metabolic needs of the heart muscle. Stable angina is the most common, while the unstable angina is less frequent. Tumor necrosis factor alpha (TNF-alpha) is a pleiotropic cytokine plays a vital function in the immune response regulation. TNF gene cluster contains many polymorphisms; the most commonly investigated polymorphism is the rs1800629 SNP. This SNP, located at - 308 position with regard to the TNF promoter region, replaces guanine (G) with adenine (A), with the allelic types - 308 G/A, and has been linked to a variety of inflammatory condition and autoimmune diseases. The - 308 G/A SNP was investigated in AP and interconnected to the TNF level to figure out the responsibilities of TNF-alpha gene polymorphism in the pathogenesis of AP.MethodThe current work design as a case-control study that involves 300 participant divided to 200 patients evaluated as (stable angina n = 100 and unstable angina n = 100) compared with 100 apparently healthy control subjects. The serum level of TNF-alpha was assessed via enzyme-linked immunosorbent assay (ELISA)/sandwich method. The genotype and allele frequency distribution of TNF-alpha rs1800629 gene polymorphism were investigated by TaqMan probe of allelic discrimination method.ResultsThe levels of TNF-alpha were significantly higher in patients with stable and unstable angina pectoris in comparison with controls. The deviation from Hardy-Weinberg equilibrium (HWE) of TNF-alpha genotypes was obvious in control and unstable angina pectoris groups. Moreover, the significant differences between patients with AP and controls under the five genetic models consider the association between TNF-alpha (rs1800629) - 308 G/A and AP with OR > 1. However, data analysis of allelic and genotypic of (rs1800629) - 308 G/A revealed higher significantly differences of GG homozygous and GA heterozygous proportions between stable angina patients and control. The A allele was more represented as etiological allele, and G allele was represented as protective allele. The serum levels of TNF-alpha were significantly higher in subjects with genetically mutated AA genotypes than in subjects with wild GG genotypes in the study groups. ROC curve analysis found the best cutoff value of TNF-alpha level was 77.25 pg/ml.ConclusionAs the results, our data observed a linked of TNF-alpha (rs1800629) - 308 G/A genetic variant with angina pectoris patients, and the A allele has been linked to the production or expression of TNF-alpha serum level and represented an etiological factor of angina pectoris.

Project description:OBJECTIVE:Several published studies have investigated the association between the -308G/A (rs1800629) polymorphism in the tumor necrosis factor-? (TNF-?) gene and the risk of dilated cardiomyopathy (DCM). However, the TNF-? gene polymorphism has a controversial role in the pathogenesis of DCM among different populations. In the present study, a meta-analysis was performed to resolve this inconsistency. METHODS:Potentially eligible papers reporting an association between the TNF-? rs1800629 polymorphism and DCM susceptibility were searched in 4 databases including PubMed, EMBASE, Chinese Biomedical Database (CBM), and the Cochrane Library up to April 1, 2018. The odds ratio (OR) with its 95% confidence interval (CI) was used to estimate the strength of the associations. Subgroup analysis based on the ethnicity, studies with or without ischemic and valvular DCM was conducted. Publication bias detection was conducted using Begg test. RESULTS:Nine papers detailing case-control studies were included, reporting a total of 1339 DCM cases and 1677 healthy controls. The meta-analysis results indicated that TNF-? rs1800629 was associated with increased DCM susceptibility in the populations studied under the heterozygous model (AG vs GG: OR?=?1.91, 95% CI?=?1.05-3.50, P?=?.035) and dominant model (AG?+?AA vs GG: OR?=?1.87, 95% CI?=?1.01-3.45, P?=?.046). In the subgroup analysis for ethnicity, rs1800629 polymorphism was significantly associated with the susceptibility of DCM for Asians under the 5 models (A vs G: OR?=?2.87, 95% CI?=?1.56-5.30, P?=?.001; AA vs GG: OR?=?3.95, 95% CI?=?1.13-13.82, P?=?0.031; AG vs GG: OR?=?3.8, 95% CI?=?1.57-9.19, P?=?.003; AA vs GG?+?AG: OR?=?2.51, 95% CI?=?1.41-4.49, P?=?.002; AG?+?AA vs GG: OR?=?3.77, 95% CI?=?1.54-9.20, P?=?.004). CONCLUSION:There may be a moderate association between TNF-? rs1800629 polymorphism and DCM susceptibility in the whole populations studied; however, TNF-? rs1800629 polymorphism was significantly associated with the susceptibility of DCM for Asians, which indicates that such associations may be different between ethnicities.

Project description:Background and objectiveThe association between TNF-α -308 G/A polymorphism and COPD remains controversial due to insufficiently strict study designs and small group sizes among different studies. In the present study, a meta-analysis update which followed a stricter procedure was performed to obtain a clearer understanding of this association.MethodsA comprehensive database search was conducted to identify the case-control studies published up to July 2015 which reported an association between the TNF-α -308 G/A polymorphism and COPD risk. Data were extracted to calculate pooled odds ratios with 95% confidence intervals under the most appropriate genetic and allelic models. Sensitivity was analyzed, and heterogeneity as well as publication bias was assessed.ResultsThirty-eight eligible studies, comprising 3,951 COPD cases and 5,110 controls, were included in this study, among which 22 studies comprising 2,067 COPD cases and 2,167 controls were performed in Asians, and 16 studies comprising 1,884 COPD cases and 2,943 controls were in non-Asians. The overall result showed that TNF-α -308 G/A polymorphisms were significantly associated with increased COPD risk in both the codominant genetic and allelic models. Individuals with the GA or AA genotype were more susceptible to COPD development than those with the GG genotype. In addition, individuals with the AA genotype were more susceptible to developing COPD than those with the GA genotype. The subgroup analysis stratified by ethnicity supported the results in Asians but not in non-Asians. However, no association was found between TNF-α -308 G/A polymorphisms and COPD susceptibility either in Asians or in non-Asians in the meta-analysis conducted with restriction to former/current smokers.ConclusionThe present meta-analysis suggested that the TNF-α -308 G/A polymorphism was associated with an increased risk of COPD among Asians but not in non-Asians. Furthermore, individuals with the AA genotype of TNF-α -308 were more susceptible to developing COPD.

Dataset Information

TNF-? -308 G?>?A (rs1800629) Polymorphism is Associated with Celiac Disease: A Meta-analysis of 11 Case-Control Studies.

Publications

TNF-α -308 G > A (rs1800629) Polymorphism is Associated with Celiac Disease: A Meta-analysis of 11 Case-Control Studies.

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