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First Degree Relatives (FDRs) of Patients with Celiac Disease Harbour an Intestinal Transcriptomic Signature that Might Protect Them from Enterocyte Damage

ABSTRACT: First Degree Relatives (FDRs) of Patients with Celiac Disease Harbour an Intestinal Transcriptomic Signature that Might Protect Them from Enterocyte Damage

PROVIDER: PRJNA439287 | ENA |

REPOSITORIES: ENA

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First Degree Relatives (FDRs) of Patients with Celiac Disease Harbour an Intestinal Transcriptomic Signature that Might Protect Them from Enterocyte Damage

Project description:Patients with Celiac Disease, first degree relatives of celiac patients and control groups displayed significant differential gene expression.

2019-03-21 | GSE112102 | GEO

First Degree Relatives of Patients with Celiac Disease Harbour an Intestinal Transcriptomic Signature that Might Protect them from Enterocyte Damage.

Project description:IntroductionCeliac disease (CeD) is an autoimmune enteropathy which affects approximately 0.7% of the global population. While first-degree relatives (FDR) of patients with CeD have a 7.5% risk of developing enteropathy, many remain protected. Therefore, intestinal mucosa of FDR might have protective compensatory mechanisms against immunological injury. We have explored the protective mechanisms that may be active in intestinal mucosa of FDR.MethodsIntestinal mucosal biopsies (4-5 pieces) from treatment naïve patients with CeD (n = 12), FDR (n = 12) (anti-tTG negative) and controls (n = 12) (anti-tTG negative) were obtained from each individual and subjected to microarray analysis using HT-12-v4 Human Expression BeadChips (Illumina). Differential gene expression analysis was carried out among CeD, FDR and controls; and resulting gene lists were analyzed using gene ontology and pathway enrichment tools.ResultsPatients with CeD, FDR and control groups displayed significant differential gene expression. Thirty seven genes were upregulated and 372 were downregulated in the intestinal mucosa of FDR in comparison to CeD and controls. Pseudogenes constituted about 18% (315/1751) of FDR differentially expressed genes, and formed "clusters" that associated uniquely with individual study groups. The three study groups segregated into distinct clusters in unsupervised (PCA) and supervised (random forests) modelling approaches. Pathways analysis revealed an emphasis on crypt-villous maintenance and immune regulation in the intestinal mucosa of FDR.ConclusionsOur analysis suggests that the intestinal mucosa of celiac FDR consist of a unique molecular phenotype that is distinct from CeD and controls. The transcriptomic landscape of FDR promotes maintenance of crypt-villous axis and modulation of immune mechanisms. These differences clearly demonstrate the existence of compensatory protective mechanisms in the FDR intestinal mucosa.

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Expression analysis in intestinal mucosa of genes under association peaks in celiac disease

Project description:Celiac disease is a chronic immune-mediated disorder with an important genetic component. To date, there are 57 independent association signals from 39 non-HLA loci, and a total of 66 candidate genes have been proposed. We aimed to scrutinize the functional implication of 45 of those genes by analyzing their expression in the disease tissue of celiac patients (at diagnosis/treatment) compared to non-celiac controls. The sample set consisted of 15 CD children at diagnosis (on a gluten-containing diet, with CD associated antibodies, atrophy of intestinal villi and crypt hyperplasia), and the same patients in remission after being treated with GFD for >2 years (asymptomatic, antibody negative, and normalized intestinal epithelium at that time), plus 15 tissue samples from non-celiac individuals not suffering from inflammation at the time of endoscopy used as controls

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