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Evaluation of IL-12A, IL-12B, IL-23A and IL-27 mRNA expression level genes in peripheral mononuclear cells of inflammatory bowel disease patients in an Iranian population.

ABSTRACT: Aim:Aim of this study was to compare the gene expression of Interleukin 12 members in two phase of IBD. Background:Inflammatory bowel disease (IBD) is a well-known gastrointestinal disorder in the world that fluctuates between remission and flare-up phases. Each of these phases has an individual immune system response profile. Therefore, analyzing the interleukins (IL) expression status improves the diagnosis and the classification of the IBD cases. Methods:In this a case-control study, among 400 patients whom admitted to the IBD clinic, forty nine IBD patients were included. Patients were divided into three categories based on 1) the phase of the disease, 2) the type of IBD, Ulcerative colitis (UC) or Crohn's disease (CD), and 3) the therapeutic pathways. Using the real-time PCR method, the expression levels of IL-12A, IL-12B, IL-23A, and IL-27 were examined in the peripheral blood mononuclear cell (PBMC) and compared to the pre-described subgroups. Results:the data showed upregulation in the expression levels of IL-12A and IL-12B in the remission phase in comparison with the flare-up. However, no significant changes were obtained from the evaluation of IL-23A and IL-27. In addition, the mRNA levels of the target genes in the subgroups of Category 2 as well as Category 3 were similar. Conclusion:Our results showed that expression patterns of the IL-12A and IL-12B genes varied between the remission and flare-up phases for the IBD patients, and may be considered as potential biomarkers for the detection and the classification of IBD cases.

SUBMITTER: Norouzinia M

PROVIDER: S-EPMC6347999 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Project description:BackgroundIrritable bowel syndrome (IBS) is a stress-sensitive disorder. Environmental factors including stress can trigger epigenetic changes, which have not been well-studied in IBS. We performed a pilot study investigating genome-wide DNA methylation of IBS patients and healthy controls (HCs) to identify potential epigenetic markers and associated pathways. Additionally, we investigated relationships of epigenetic changes in selected genes with clinical traits.MethodsTwenty-seven IBS patients (59% women; 10 IBS-diarrhea, 8 IBS-constipation, 9 IBS-mixed) and 23 age- and sex-matched HCs were examined. DNA methylation from peripheral blood mononuclear cells (PBMCs) was measured using HM450 BeadChip, and representative methylation differences were confirmed by bisulphite sequencing. Gene expression was measured using quantitative PCR. Gastrointestinal (GI) and non-GI symptoms were measured using validated questionnaires. Associations were tested using non-parametric methods.Key resultsGenome-wide DNA methylation profiling of IBS patients compared with HCs identified 133 differentially methylated positions (DMPs) (mean difference ≥10%; p < 0.05). These genes were associated with gene ontology terms including glutathione metabolism related to oxidative stress and neuropeptide hormone activity. Validation by sequencing confirmed differential methylation of subcommissural organ (SCO)-Spondin (SSPO), glutathione-S-transferases mu 5 (GSTM5), and tubulin polymerization promoting protein genes. Methylation of two promoter CpGs in GSTM5 was associated with epigenetic silencing. Epigenetic changes in SSPO gene were positively correlated with hospital anxiety and depression scores in IBS patients (r > 0.4 and false discovery rate <0.05).Conclusions & inferencesThis study is the first to comprehensively explore the methylome of IBS patients. We identified DMPs in novel candidate genes which could provide new insights into disease mechanisms; however, these preliminary findings warrant confirmation in larger, independent studies.

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Evaluation of IL-12A, IL-12B, IL-23A and IL-27 mRNA expression level genes in peripheral mononuclear cells of inflammatory bowel disease patients in an Iranian population.

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