Ontology highlight
ABSTRACT:
PROVIDER: PRJNA936674 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23586500_1.fastq.gz | Fastqsanger.gz | |||
| SRR23586500_2.fastq.gz | Fastqsanger.gz | |||
| SRR23586600_1.fastq.gz | Fastqsanger.gz | |||
| SRR23586600_2.fastq.gz | Fastqsanger.gz | |||
| SRR23586501_1.fastq.gz | Fastqsanger.gz |
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Project description:The alpha gliadins are a complex group of proteins with very similar sequences that comprise about 15-20% of the total flour protein and contribute to the functional properties of wheat flour dough. Some alpha gliadins also contain immunodominant epitopes relevant to celiac disease, a chronic autoimmune disease that affects nearly 1.4% of the worldwide population. In an attempt to reduce the immunogenic potential of wheat flour in the U.S. spring wheat cultivar Butte 86, RNA interference was used to silence a subset of alpha gliadin genes encoding proteins containing celiac disease epitopes. Two of the resulting transgenic lines were analyzed in detail by quantitative two-dimensional gel electrophoresis combined with tandem mass spectrometry. Although only some genes were targeted by the RNA interference construct, all alpha gliadins were effectively silenced in the transgenic plants. Some off-target silencing of high molecular weight glutenin subunits also was detected in both transgenic lines even though there was no homology with the target sequence. Reactivities of IgG and IgA serum antibodies from a cohort of patients with confirmed cases of celiac disease were decreased in flour from the two transgenic lines relative to the non-transgenic line. However, functional properties of the flour were also altered in the transgenic lines as evidenced by decreases in both mixing times and SDS sedimentation values. Although it may be possible to reduce the immunogenic potential of the flour and retain the viscoelastic properties essential for the utilization of wheat by eliminating only the most immunogenic alpha gliadins, the data suggest that it will be very difficult to selectively silence specific genes within families as complex as the wheat alpha gliadins.
2020-02-28 | PXD016930 | Pride
Project description:Study of the effects of re-exposure to gliadin of intestinal biopsies from normalized celiac patients (>2 years on gluten free diet). Comparison of the expresson profile in biopsy portions incubated with 10ug/ml gliadin versus without gliadin for 4 hours.
2009-06-01 | E-MEXP-1823 | biostudies-arrayexpress
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:Gliadin triggers T-cell mediated immunity in celiac disease, and has cytotoxic effects on enterocytes mediated through obscure mechanisms. In addition, gliadin transport mechanisms, potential cell surface receptors and gliadin-activated downstream signaling pathways are not completely understood. In order to screen for novel downstream gliadin target genes we performed a systematic whole genome expression study on intestinal epithelial cells. Undifferentiated Caco-2 cells were exposed to pepsin- and trypsin- digested gliadin (PT-G), a blank pepsin-trypsin control (PT) and to a synthetic peptide corresponding to gliadin p31-43 peptide for six hours. RNA from four different experiments was used for hybridization on Agilent one color human whole genome DNA microarray chips. The microarray data were analyzed using the Bioconductor package LIMMA. Genes with nominal p < 0.01 were considered statistically significant. Compared to the untreated cells 1705, 1755 and 211 probes were affected by PT-G, PT and p31-43 respectively. 46 probes were significantly different between PT and PT-G treated cells. Among the p31-43 peptide affected probes, 10 and 21 probes were affected by PT-G and PT respectively. Only PT-G affected genes could be validated by quantitative real-time polymerase chain reaction. All the genes were, nonetheless, also affected to a comparable level by PT treated negative controls. In conclusion, we could not replicate previously reported direct effects of gliadin peptides on enterocytes. The PT-G affected genes in the microarray analysis were validated by qRT-PCR, however these genes were also affected by PT treated negative controls suggesting that certain epitopes derived from pepsin and trypsin may also affect epithelial cell gene transcription. Our study demonstrates novel non-enzymatic effects of pepsin and trypsin on cells and calls for proper controls in pepsin and trypsin digested gliadin experiments. It is conceivable that gliadin effects on enterocytes are secondary mediated through oxidative stress, NFkB activation and IL-15 up-regulation. In total, 16 samples were analyzed of which 4 were control (MED) samples, 4 samples of p31-43 treatment, 4 samples of PT treatmetn and 4 samples of PT-G treatment
2013-03-21 | E-GEOD-45357 | biostudies-arrayexpress
Project description:Background Celiac disease (CeD) is an autoimmune disorder triggered by gluten, with gliadin as the primary antigen. Therapies targeting gliadin to induce antigen-specific immune tolerance are of significant interest. This study investigates the therapeutic potential of a novel rapamycin-gliadin composite nanoparticle (PLN-GR) in enhancing Kupffer cell-mediated hepato-splenic dialogue to promote gluten tolerance in CeD. Methods Rapamycin-gliadin composite nanoparticles were synthesized using a precipitation self-assembly method and characterized for size, zeta potential, and cellular uptake. A CeD delayed-type hypersensitivity (DTH) mouse model was employed to evaluate the immunomodulatory effects of PLN-GR. Cellular biodistribution, immune phenotyping, and metabolic assessments were conducted to elucidate the nanoparticles' mechanism of action. Results Rapamycin-gliadin composite nanoparticles effectively targeted the liver and were internalized by Kupffer cells, inducing a tolerogenic phenotype. In vivo treatment with PLN-GR ameliorated systemic and intestinal inflammation in the CeD DTH mouse model, evidenced by reduced paw swelling and intestinal histopathology. The nanoparticles induced a metabolic shift from glycolysis to oxidative phosphorylation in macrophages, associated with increased itaconate production. This metabolic reprogramming was linked to an increase in PD-L1+ tolerogenic dendritic cells and a decrease in Th1 cell counts in the spleen. Conclusion The study demonstrates that rapamycin-gliadin nanoparticles can induce antigen-specific tolerance in CeD by modulating hepatic and splenic immune responses. The findings suggest a potential therapeutic strategy for CeD by enhancing immunometabolic reprogramming and inter-organ communication.
2025-07-30 | GSE275197 | GEO
Project description:Background and aims: Celiac disease is provoked by gluten exposure, but the resultant pathogenic process in the duodenum is not well understood. We aimed to define the core celiac transcriptomic signature and pathologic pathways in pre-treatment diagnostic duodenum biopsies. Methods: We use mRNAseq to define pre-treatment diagnostic duodenum gene expression in 54 pediatric celiac patients and non-celiac controls, and we validate our key findings in an independent cohort of 40 participants. We further define similar and divergent genes and pathways in 177 Crohn disease patients and controls. Results: We observe a marked suppression of mature epithelial metabolic functions in celiac patients, overlapping substantially with the Crohn signature. A marked adaptive immune response was noted for the up-regulated signature including interferon response, alpha-beta, and gamma-delta T-cells that overlapped to some extant with the Crohn signature. However, we identified a celiac specific signature linked to increased cell proliferation, nuclear division, and cell cycle activity that was localized primarily to the epithelia as noted by CCNB1 and Ki67 staining. Lastly, we demonstrate the utility of the transcriptomic date to correctly classify disease or healthy states in the discovery and validation cohorts. Conclusion: Our data provide insights into celiac pathogenesis and can stimulate new approaches to address this highly prevalent condition.
2020-04-10 | GSE131705 | 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:We use targeted bisulfite PCR and next-generation 454 sequencing of multiple amplicons to analyze the association of cis-regulated allele-specific methylation (ASM) with multiple complex disease-associated variants in a population of 82 individuals. We detect ASM at four variants implicated in complex phenotypes such as ulcerative colitis and AIDS progression disease (rs10491434), Celiac disease (rs2762051), Crohn’s disease, IgA nephropathy and early-onset inflammatory bowel disease (rs713875) and height (rs6569648). 82 samples analysed
2014-07-01 | E-GEOD-56298 | biostudies-arrayexpress