Gut microbiome of individuals with Non-celiac gluten wheat sensitivity
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PROVIDER: PRJNA1183595 | ENA |
REPOSITORIES: ENA
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Project description:Gut microbiota and mycobiota composition associated with Non-celiac gluten wheat sensitivity Raw sequence reads
| PRJNA701870 | ENA
Project description:While the antigenic specificity and pathogenic relevance of immunologic reactivity to gluten in celiac disease have been extensively researched, the immune response to non-gluten proteins of wheat has not been characterized. We aimed to investigate the level and molecular specificity of antibody response to wheat non-gluten proteins in celiac disease. Serum samples from patients and controls were screened for IgG and IgA antibody reactivity to a non-gluten protein extract from the wheat cultivar Triticum aestivum 'Butte 86'. Antibodies were further analyzed for reactivity to specific non-gluten proteins by immunoblotting, following two-dimensional gel electrophoretic separation. Immunoreactive molecules were identified by tandem mass spectrometry. Compared with healthy controls, patients exhibited significantly higher levels of antibody reactivity to non-gluten proteins. The main immunoreactive non-gluten antibody target proteins were identified as serpins, purinins, α-amylase/protease inhibitors, globulins, and farinins. Assessment of reactivity towards purified recombinant proteins further confirmed the presence of antibody response to specific antigens. The results demonstrate that, in addition to the well-recognized immune reaction to gluten, celiac disease is associated with a robust humoral response directed at a specific subset of the non-gluten proteins of wheat
2014-10-05 | MSV000078884 | MassIVE
Project description:Dietary gluten proteins (prolamins) from wheat, rye, and barley are the driving forces behind celiac disease, an organ-specific autoimmune disorder that targets both the small intestine and organs outside the gut. In the small intestine, gluten induces inflammation and a typical morphological change of villous atrophy and crypt hyperplasia. Gut lesions improve and heal when gluten is excluded from the diet and the disease relapses when patients consume gluten. Oral immune tolerance towards gluten may be kept for years or decades before breaking tolerance in genetically susceptible individuals. Celiac disease provides a unique opportunity to study autoimmunity and the transition in immune cells as gluten breaks oral tolerance. Seventy-three celiac disease patients on a long-term gluten-free diet ingested a known amount of gluten daily for six weeks. A peripheral blood sample and intestinal biopsies were taken before and six weeks after initiating the gluten challenge. Biopsy results were reported on a continuous numeric scale that measured the villus height to crypt depth ratio to quantify gluten-induced gut mucosal injury. Pooled B and T cells were isolated from whole blood, and RNA was analyzed by DNA microarray looking for changes in peripheral B- and T-cell gene expression that correlated with changes in villus height to crypt depth, as patients maintained or broke oral tolerance in the face of a gluten challenge.
2017-01-27 | GSE87629 | GEO
Project description:Here is reported the first study of transcriptome analyses using the Illumina HiSeq 4000 platform for three kinds of wheat (G represents Strong gluten wheat, Z represents middle gluten wheat,R represents weak gluten wheat). The variation of wheat varieties with different gluten content is mainly shown in the content of gluten, flour is divided into high gluten powder ( > 30%), medium gluten powder (26%-30%) and low gluten powder ( < 20%), according to the wet gluten content. In total, over 102.6 Gb clean reads were produced and 114, 621 unigenes were assembled; more than 59,085 unigenes had at least one significant match to an existing gene model. Differentially expressed gene analysis identified 2339 and 2600 unigenes which were expressed higher or lower among strong gluten, middle gluten and weak gluten wheat. After functional annotation and classification, three dominant pathways including protein isomerase, antioxidase activity and energy metabolism, and 410 unigenes related to gluten strength polymerization of wheat were discovered. In strong-gluten wheat, low molecular weight subunit content is higher than weak-gluten wheat, and the activity of cysteine synthase and isomerase is increased, which may promote the cross-linking of low molecular weight protein to high molecular weight protein. Meanwhile, POD enzyme strengthens gluten network and CAT enzyme affects gluten polymerization, along with higher ATPase activity, which will provides energy for protein polymerization reaction in comparison of strong-gluten wheat and weak-gluten wheat. The accuracy of these RNA-seq data was validated by qRT-PCR analysis. These data will extend our knowledge of quality characteristics of wheat and provide a theoretical foundation for molecular mechanism research of wheat.
2020-09-03 | GSE122699 | GEO
Project description:Analysis of the influence of celiac disease-associated bacteria and gluten on intestinal epithelial cells
2017-09-01 | GSE103374 | GEO
Project description:Study on the effects of long term, dietary, consumption of gliadin (gluten) in patients with celiac disease. Comparison of expression profiles of biopsies from normalized patients treated with gluten-free diet >2 years (FU-follow-up samples) versus biopsies from patients with active disease (Dx-at diagnosis samples)
2009-06-01 | E-MEXP-1828 | biostudies-arrayexpress
Project description:Background & Aims: Traditional celiac disease diagnostics based on histomorphometric evaluations are liable to misinterpretations due to the common technical flaws e.g. wrong orientation of the biopsy and subjective errors are relatively common e.g. interobserver errors. We envisioned that there is a need for molecular histomorphometric tool that obviates these error sources yielding an objective ratio instead. Gene expression determine the state of a tissue, so the changes in expression may be associated with the severity of lesions during CD and can be used to classify it. Methods: 15 CD patients, who have been at least one year on gluten-free diet, were enrolled. All participants were biopsied before and after the gluten challenge (10 weeks, 4 grams of gluten daily). 6 healthy non-CD individuals were included as controls. Biopsies were taken on PAXgene biological fixative and embedded in paraffin and Vh/Cd ratio was assessed. RNA was extracted from the same sections and subjected to genome-wide 3’RNA-sequencing. Sequencing data was used to determine differentially expressed genes and regression model, that successfully describes the mucosal damage, was created and tested in independent material. Results: 167 differentially expressed genes were identified in healthy vs. treated CD comparisons with 117 genes downregulated and 50 genes upregulated. 415 differentially expressed genes were identified in Post gluten challenge to Treated CD comparisons with 195 genes downregulated and 220 genes upregulated. 119 genes whose expression highly correlates to Vh/Cd ratio (Spearman’s rank correlation coefficient, |rho|>0.7) were identified. Gene ontology analyses show that genes involved in cellular response to cytokines, including interferons, were over-represented. Stepwise regression allowed us computationally cut down the number of genes, that describe Vh/Cd ratio changes, to 7 and IELs number to 5. Created models describe 98.9% of observed Vh/Cd and 97.5% of IELs number variabilities; there is a strong correlation between the model’s predicted and observed ratios. Conclusions: Adoption of molecular histomorphometry, with our selected set of target genes, is quantitative and reliable way of estimating gluten-induced mucosal injury and inflammation. By including this technology one can overcome the typical shortcomings common in celiac disease diagnostics based on traditional histomorphometry analyses alone. Likewise, molecular histomorphometry is a promising instrument when incorporated in clinical trials where assessing drug efficacy on mucosal health is paramount. In addition, despite deemed healthy, based on traditional histomorphometric analyses, celiac patients on gluten free diet have significantly distinctive molecular histomorphometric pattern when compared to healthy controls.
2020-07-21 | GSE145358 | GEO
Project description:Analysis of the influence of celiac disease-associated bacteria and gluten on intestinal epithelial cells
2017-08-26 | GSE103100 | GEO
Project description:Gluten proteins are responsible for the unique viscoelastic properties of wheat dough, but they also trigger the immune response in celiac disease patients. RNA interference (RNAi) wheat lines with strongly silenced gliadins were obtained to reduce the immunogenic response of wheat. The E82 line presents the highest reductions of gluten, but other grain proteins increased, maintaining a total nitrogen content comparable to that of the wild type. To better understand the regulatory mechanisms in response to gliadin silencing, we carried out a transcriptomic analysis of grain and leaf tissues of the E82 line during grain filling. A network of candidate transcription factors (TFs) that regulates the synthesis of the seed storage proteins (SSPs), α-amylase/trypsin inhibitors, lipid transfer proteins, serpins, and starch in the grain was obtained. Moreover, there were a high number of differentially expressed genes in the leaf of E82, where processes such as nutrient availability and transport were enriched. The source-sink communication between leaf and grain showed that many down-regulated genes were related to protease activity, amino acid and sugar metabolism, and their transport. In the leaf, specific proline transporters and lysine-histidine transporters were down- and up-regulated respectively. Overall, the silencing of gliadins in the RNAi line is compensated mainly with lysine-rich globulins, which are not related to the proposed candidate network of TFs, suggesting that these proteins are independently regulated to the other SSPs. Results reported here can explain the protein compensation mechanisms and contribute to decipher the complex TF network operating during grain filling.
2022-07-26 | GSE199525 | GEO
Project description:Celiac disease (CeD) is an intestinal immune-mediated disorder caused by gluten ingestion in genetically predisposed subjects. CeD is characterized by villous atrophy, altered intestinal permeability, crypt hyperplasia and innate and adaptive immune response. This study aimed to develop and validate the use of intestinal organoids from celiac patients to study CeD. A repository of organoids from duodenum of non-celiac and celiac patients was generated and characterized accordingly to standard procedures. RNA-seq analysis was employed to study the global gene expression program of CeD (n=3) and non-CeD (n=3) organoids sets. While the three celiac derived organoids shared similar transcriptional signatures the NC samples set appeared more heterogeneous. We found 486 genes differentially expressed between the two groups. Of them, 299 genes were downregulated (FC<2; FDR<0.05) and 187 were upregulated in CeD (FC >2; FDR<0.05). We observed CeD organoids had significantly altered expression of genes associated with barrier function, innate immunity, and stem cell function.
2019-05-29 | GSE113492 | GEO