Human metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA210341 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Metagenome data from soil samples were collected at 0 to 10cm deep from 2 avocado orchards in Channybearup, Western Australia, in 2024. Amplicon sequence variant (ASV) tables were constructed based on the DADA2 pipeline with default parameters.
2025-06-15 | GSE298403 | GEO
Project description:Dietary intake of fruits and vegetables (FV) has been inversely associated with lower risk of ulcerative colitis. A pig model was used to evaluate the impact of feeding FV on the host response to dextran sulfate sodium (DSS)-induced colitis. Methods: Six-week-old pigs were fed a grower diet alone or supplemented with lyophilized FV equivalent to the half (half-FV) or full (full-FV) daily levels recommended for humans by the Dietary Guidelines for Americans (DGA). Pigs were fed a 1) grower diet alone (negative control), 2) grower diet and orally treated with 4% DSS for 10 days to induce colitis (positive control), 3) half-FV diet treated with 4% DSS or 4) full-FV diet treated with 4% DSS. Pigs were monitored for the development of clinical signs of colitis. Proximal colon (PC) contents and mucosa (PCM) were collected for gut metagenome, tissue transcriptome and histopathological analysis. Results: Pigs fed the full-FV diet did not exhibit diarrhea, showed less fecal occult blood (FOB), PCM crypt hyperplasia but with no differential expressed genes (DEG) or changes in PC microbiome diversity (p < 0.05). Pigs within the half-FV group exhibited increased group FOB and DEG associated with tissue remodeling, crypt and goblet cell hyperplasia in the PCM and no changes in PC microbiome diversity and two pigs exhibiting diarrhea (p < 0.05). Pigs within the DSS positive control group exhibited a reduced DEG involved with intestinal immune response and PC microbiome diversity with altered metagenome, increased group PCM erosion and FOB with persistent diarrhea in one pig (p < 0.05) Conclusions: Overall, our results showed that pigs fed a three-week full-FV supplemented diet, were resistant to DSS-induced colitis with a differential dose-dependent protective effect on host intestinal tissue and gut metagenome when exposed to an inflammatory challenge.
2026-04-01 | GSE317287 | 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
Project description:In vitro models of autoimmunity are constrained by an inability to culture affected epithelium alongside the complex tissue-resident immune microenvironment. Celiac disease (CeD) is an autoimmune disease where dietary gluten-derived peptides bind the MHC- II molecules HLA-DQ2 or -DQ8 to initiate immune-mediated duodenal mucosal injury. Here, we generated air-liquid interface (ALI) duodenal organoids from endoscopic biopsies that preserve epithelium alongside native mesenchyme and tissue-resident immune cells as a unit without requiring reconstitution. The ALI organoid immune diversity spanned T, B, plasma, NK and myeloid cells with extensive T and B cell receptor repertoires. HLA-DQ2.5-restricted gluten peptides selectively instigated epithelial destruction in HLA-DQ2.5-expressing CeD patient organoids, which was antagonized by MHC-II or NKG2C/D blockade. Gluten epitopes stimulated a CeD organoid network response in lymphoid and myeloid subsets alongside anti-TG2 autoantibody production. Functional studies in CeD organoids revealed IL-7 as a novel gluten-inducible pathogenic modulator which regulated CD8+ T cell-NKG2C/D expression and was necessary and sufficient for epithelial destruction. Further, endogenous IL-7 was markedly induced in patient biopsies from active CeD versus remission disease, predominantly in lamina propria mesenchyme. By preserving epithelium alongside diverse immune populations, this human in vitro CeD model recapitulates gluten-dependent pathology, facilitates mechanistic investigation, and establishes proof-of-principle for organoid modeling of autoimmunity.
2024-07-12 | GSE200075 | GEO
Project description:Celiac disease (CeD) is an immune-mediated chronic enteropathy caused by gluten exposure in HLA-DQ2 and/or -DQ8 positive individuals. The hallmarks of CeD include increased intraepithelial lymphocytes and villous atrophy. Clinically, a small subset of individuals with elevated serum tissue transglutaminase antibody (TTG) concentrations but unremarkable duodenal mucosa at initial endoscopy may progress to CeD over time. We hypothesize that these rare CeD precursor cases can allow us to interrogate histologic and molecular signatures to predict those who subsequently develop CeD, and to study the final cascade into overt lesions in CeD.
2025-08-06 | GSE273155 | GEO
Project description:Background and Aims: Celiac disease (CeD) is an autoimmune disease triggered by dietary gluten in genetically predisposed individuals. Deamidation of gluten peptides by the CeD autoantigen and enzyme transglutaminase 2 (TG2) is central to the pathogenesis of CeD. Inhibition of TG2 with the specific inhibitor ZED1227 effectively prevents gluten-induced histological damage in CeD patients. Here we aimed to explore the blood DNA methylomic changes in ZED1227-treated CeD patients undergoing a gluten challenge. Results: Drug treatment revealed consistent patterns suggesting normalization of the DNA methylome indicating that ZED1227 attenuated the systemic responses to gluten challenge. Conclusions: These findings provide evidence that ZED1227 can significantly prevent the gluten-induced CeD-associated systemic changes. Clinical trial: EudraCT 2017-002241-30
2026-06-18 | GSE319777 | GEO
Project description:We applied 10X Genomic scRNAseq to profile cell population within human intestinal organoids infected with coxsackievirus B1. The intestinal epithelium represents the first line of defense in the gastrointestinal tract, forming an essential barrier that, when compromised, renders individuals with celiac disease (CeD) susceptible to mucosal damage. By connecting viral infections and gluten challenges, this study sheds light on a mechanistic bridge between viral infection and gluten peptide modification, a critical step in the onset of CeD.
2026-05-31 | GSE333246 | GEO
Project description:The pathogenesis of celiac disease (CeD) remains incompletely understood. Traditional diagnostic techniques for CeD include serological testing and endoscopic examination; however, they have limitations. Therefore, there is a need to identify novel noninvasive biomarkers for CeD diagnosis. We analyzed duodenal and plasma samples from CeD patients by four-dimensional data-dependent acquisition (4D-DIA) proteomics. Differentially expressed proteins (DEPs) were identified for functional analysis and to propose blood biomarkers associated with CeD diagnosis. In duodenal and plasma samples, respectively, 897 and 140 DEPs were identified. Combining weighted gene co-expression network analysis(WGCNA) with the DEPs, five key proteins were identified across three machine learning methods. FGL2 and TXNDC5 were significantly elevated in the CeD group, while CHGA expression showed an increasing trend, but without statistical significance. The receiver operating characteristic curve results indicated an area under the curve (AUC) of 0.7711 for FGL2 and 0.6978 for TXNDC5, with a combined AUC of 0.8944. Exploratory analysis using Mfuzz and three machine learning methods identified four plasma proteins potentially associated with CeD pathological grading (Marsh classification): FABP, CPOX, BHMT, and PPP2CB. We conclude that FGL2 and TXNDC5 deserve exploration as potential sensitive, noninvasive diagnostic biomarkers for CeD.
2024-11-15 | PXD057692 | Pride