Intestinal model
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA453619 | ENA |
REPOSITORIES: ENA
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Project description:The early-life intestinal microbiota plays a key role in shaping host immune system development. We found that a single early-life antibiotic course (1PAT) accelerated Type 1 diabetes (T1D) development in male NOD mice. The single course had strong and persistent effects on the intestinal microbiome, selecting for a highly metabolically active metagenome, with altered hepatic and serum metabolites. The exposure led to differential ileal and hepatic histone modification, and perturbed ileal gene expression, strongly affecting the normal maturational pattern. Earliest effects involved specific genes in innate immune pathways, with later effects on adaptive immunity. Microbiome analysis revealed four potential T1D-protective taxa and four T1D-accelerating taxa, and a network linking specific microbial taxa to differences in ileal gene expression was identified. This simplified animal model has improved understanding of the mechanisms by which early-life gut microbiome perturbations alter host intestinal responses, contributing to T1D.
2018-08-03 | GSE101721 | GEO
Project description:In a rat model of induced intestinal obstruction, a transcriptomic analysis was used to measure global gene expression. Rat fetuses small intestines of different stages of development (ED15, ED17, ED19 and ED21, were studied as non-operated controls and compared to upper and lower segments of rat fetuses small intestine with an induced obstruction (ligature at ED18).
2017-10-16 | E-MTAB-5981 | biostudies-arrayexpress
Project description:Increased intestinal permeability is associated to the onset of inflammatory bowel disease (IBD) since the exposition to luminal content causes an immunological response that promotes intestinal inflammation. Several studies have been shown that microRNAs (miRNAs) are involved in IBD pathogenesis. Here, we aimed to functionally characterize the role of miRNAs in the regulation of intestinal permeability. miRNA profile of intestinal epithelial cells (IECs) isolated by colon of a UC mice model were identified using microarray. To predict the target genes of modulated miRNAs, we performed a bioinformatic analysis. To validate biologically miRNA targets, we performed transient transfection experiments in HT-29, Caco2 and T84 cell lines. To assess their role in barrier function, trans-epithelial electrical resistance and dextran flux assays were used. To investigate the in vivo effect of miR-195-5p, we employed a DSS-induced colitis model in mice. We identified 18 deregulated miRNAs in IECs from UC mice model and control mice. Among them, down-regulated miR-195-5p targeted CLDN2 and are involved in altered intestinal permeability. CLDN2 expression levels were increased in UC mice models and negatively correlated with the miR-195-5p expression. We demonstrated that the gain-of-function of miR-195-5p in colonic epithelial cell lines decreased the CLDN2 levels. We in vitro confirmed that miR-195-5p was able to control the intestinal barrier integrity. We also in vivo demonstrated that miR-195-5p attenuated the colonic inflammatory response in DSS-induced colitis and reduced the colonic permeability. All together our data support a previously unreported role of miR-195-5p in intestinal permeability and provide a potential pharmacological target for new therapeutic approaches in IBD.
2022-04-27 | GSE183896 | GEO
Project description:Here, we introduce an intestinal tissue model to study human enteric infections. Our model comprises epithelial and endothelial layers, a primary intestinal collagen scaffold, and immune cells. We use Dual RNA-seq to chart the communication amongst several different cell types at the intestinal barrier and the pathogen. The results suggest that Salmonella uses its type III secretion systems to manipulate STAT3-dependent inflammatory responses locally in the epithelial compartment. Our approach promises to reveal more human-specific infection strategies employed by Salmonella and other pathogens.
2020-01-20 | GSE136717 | GEO
Project description:Intestinal ischemia-reperfusion (IR) injury is associated with high mortality rates, which have not improved in the past decades despite advanced insight in its pathophysiology using in vivo animal and human models. The inability to translate previous findings to effective therapies emphasizes the need for a physiologically relevant in vitro model to thoroughly investigate mechanisms of IR-induced epithelial injury and test potential therapies. In this study, we demonstrate the use of human small intestinal organoids to model IR injury by exposing organoids to hypoxia and reoxygenation (HR). A mass-spectrometry-based proteomics approach was applied to characterize organoid differentiation and decipher protein dynamics and molecular mechanisms of IR injury in crypt-like and villus-like human intestinal organoids.
2021-01-11 | PXD022999 | Pride
Project description:mice intestinal metagenome Metagenome
| PRJNA678884 | ENA
Project description:Intestinal polyposis, a precancerous neoplasia, results primarily from an abnormal increase in the number of crypts. Crypts contain intestinal stem cells (ISCs). Thus intestinal polyposis provides an ideal condition for studying stem cell involvement in polyp/tumor formation. Using a conditional knock-out mouse model, we found that the tumor suppressor Phosphatase of Tension homolog (PTEN) governs the proliferation rate and number of ISCs and loss of PTEN results in an excess of ISCs. In PTEN mutants, excess ISCs initiate de-novo crypt formation and crypt fission, recapitulating crypt production in fetal/neonatal intestine. Microarray studies were used to profile the changes in gene expression that occurred when PTEN was knocked out in the intestine. Experiment Overall Design: A conditional PTEN mutant allele [Groszer, M. et al. Negative regulation of neural stem/progenitor cell proliferation by the Pten tumor suppressor gene in vivo. Science 294, 2186-2189 (2001).] was combined with in interferon inducible Mx1-Cre [Kuhn, R., Schwenk, F., Aguet, M. & Rajewsky, K. Inducible gene targeting in mice. Science 269, 1427-1429 (1995).] to enable PTEN to be deleted from the intestine by administration of polyinosinicâ??polycytidylic acid (Poly I:C). PolyI:C was administered at weaning (every other day, five times total) to three PTEN mutant (Mx1-Cre positive:PTENfx/fx) and two control (Mx1-Cre negative:PTENfx/+) animals. Intestinal polyps (from PTEN mutants) and equivalent regions of intestine (from controls) were isolated 30 days after the final polyI:C injection. Microarray analysis compared the gene expression profiles of PTEN mutant polyps and control intestines. Genes were considered up-regulated or down-regulated if all of the following conditions were met: 1) There was at least a two-fold change in the average probe signal measured between controls and mutants; 2) There was no overlap between the range of mutant and control data; and 3) The control mean was outside the 95% confidence interval of the PTEN-mutant mean.
2008-06-14 | E-GEOD-6078 | biostudies-arrayexpress
Project description:Small RNA-seq profiling of a directed differentiation organoid model revealed changing microRNA landscapes of early human small intestinal development
2022-07-27 | GSE207467 | GEO