Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA152515 | ENA |
REPOSITORIES: ENA
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Project description:Age-dependent gene expression in isolated small intestinal epithelial cells (IECs)
| PRJNA152513 | ENA
Project description:A striking example of the intricate interplay between diet, microbiota, and host is the effect of inulin, a dietary fiber, on the intestinal epithelium. Ingestion of inulin triggers a wide range of epithelial effects in the colon, such as enhanced proliferation, increased production of mucus and antimicrobial peptides, as well as systemic effects on host metabolism and immune function that are dependent on microbiota-derived molecules. In this study, we investigated the impact of inulin on two critical aspects of diet-microbiota-host interactions: intestinal hypoxia and the modulation of hypoxia-inducible factor (HIF)-1 signaling in intestinal epithelial cells (IECs) in mice colon. To achieve this, we employed a multilayered and multi-omics approach, including dietary interventions, in vitro analysis using intestinal organoids, and both genetic and pharmacological interventions. We found that inulin intake enhances intestinal hypoxia, resulting in the stabilization of HIF-1 in IECs, an effect that is both microbiota- and host-dependent. Our study revealed that HIF-1 plays a key role in regulating IEC proliferation and intestinal stem cell (ISC) function. These changes are associated with HIF-1-dependent metabolic alterations in IECs. Our findings uncover a novel mechanism by which HIF-1 acts in the colon: it acts as a molecular brake, modulating cell proliferation in a microbiota-dependent manner and through metabolic reprogramming, highlighting the complexity of the diet-microbiota-host interactions in the gut.
2025-08-22 | PXD059757 | Pride
Project description:Inflammatory injury to the intestine triggers a reprogramming of the intestinal epithelium to a fetal-like state, facilitating rapid restoration of the epithelial barrier. Although the intestinal microbiota is a key modulator of inflammation, its role in driving epithelial fetal-like reversion and promoting restitution remains unclear. Using irradiation (IR) injury as a model for small intestinal epithelium restitution, we found that the intestinal microbiota accelerated epithelial restitution by amplifying a repair-associated inflammatory response that promoted the emergence of fetal-like intestinal epithelial cells (IECs), marked by Ly6a and Clu. NOD2, the strongest genetic link to the development of Crohn’s disease, was expressed in fetal-like IECs following injury. Notably, stimulation of NOD2 by its peptidoglycan ligand in an ileal organoid model potentiated an inflammatory gene signature characterized by interferon (IFN) signaling, coinciding with enterocyte recovery. NOD2 deficiency exacerbated epithelial apoptosis following IR injury, while epithelial-specific NOD2 signaling promoted the emergence of fetal-like IECs and enhanced epithelial proliferation. Together, these results identify a critical role for microbiota and microbial sensing by NOD2 in controlling the fate of fetal-like IECs following injury, thereby contributing to the protective effect of this microbial sensor during intestinal inflammation.
2026-04-29 | GSE295472 | GEO
Project description:We profiled transcriptome and accessible chromatin landscapes in intestinal epithelial cells (IECs) from mice reared in the presence or absence of microbiota. We show that regional differences in gene transcription along the intestinal tract were accompanied by major alterations in chromatin organization. Surprisingly, we discovered that microbiota modify host gene transcription in IECs without significantly impacting the accessible chromatin landscape. Instead, microbiota regulation of host gene transcription might be achieved by differential expression of specific TFs and enrichment of their binding sites in nucleosome depleted CRRs near target genes. Our results suggest that the chromatin landscape in IECs is pre-programmed by the host in a region-specific manner to permit responses to microbiota through binding of open CRRs by specific TFs. mRNA and accessible chromatin (DNase-seq) profiles from colonic and ileal IECs were compared between conventionally-raised (CR), germ-free (GF), and conventionalized (CV) C57BL/6 mice.
2014-06-07 | E-GEOD-57919 | biostudies-arrayexpress
Project description:Transcriptional response of small intestinal epithelial cells (S-IECs) to bacterial monocolonization
| PRJNA345541 | ENA
Project description:Expression data from intestinal epithelial cells (IECs) [Mouse430_2 array]
| PRJNA247395 | ENA
Project description:We profiled transcriptome and accessible chromatin landscapes in intestinal epithelial cells (IECs) from mice reared in the presence or absence of microbiota. We show that regional differences in gene transcription along the intestinal tract were accompanied by major alterations in chromatin organization. Surprisingly, we discovered that microbiota modify host gene transcription in IECs without significantly impacting the accessible chromatin landscape. Instead, microbiota regulation of host gene transcription might be achieved by differential expression of specific TFs and enrichment of their binding sites in nucleosome depleted CRRs near target genes. Our results suggest that the chromatin landscape in IECs is pre-programmed by the host in a region-specific manner to permit responses to microbiota through binding of open CRRs by specific TFs.
2014-06-07 | GSE57919 | GEO
Project description:Remodeling of the gut microbiota is implicated in various metabolic and inflammatory diseases of the gastrointestinal tract. We hypothesized that the gut microbiota affects the DNA methylation profile of intestinal epithelial cells (IECs) which could, in turn, alter intestinal function. Here, we used mass spectrometry and methylated DNA capture to respectively investigate global and genome-wide DNA methylation of intestinal epithelial cells from germ-free (GF) and conventionally raised mice (CONV-R). In colonic IECs from GF mice, DNA was markedly hypermethylated. This was associated with a dramatic loss of Ten-Eleven-Translocation activity, a lower DNA methyltransferase activity and lower circulating levels of the one carbon metabolites cobalamin and folate. At the gene level, we found an enrichment for differentially methylated regions at proximity of genes regulating cytotoxicity of Natural Killer cells (FDR < 8.9E-6), notably members of the natural killer group 2 member D ligand superfamily Raet. Our results suggest that altered activity of methylation-modifying enzymes in GF mice influences the IEC epigenome at genes involved in the crosstalk between intestinal and immune cells. Epigenetic reprogramming of IECs by the gut microbiota may modulate intestinal function in diseases associated with altered gut microbiota.
2019-01-23 | GSE117434 | GEO
Project description:The intestinal epithelium plays a critical role in immune–microbiota interactions, yet its contribution to systemic autoimmunity remains unclear. Here, we identify intestinal epithelial cells (IECs) as key initiators of experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis (MS). In MS patients, IECs upregulate antigen presentation–related genes and associate with increased intestinal Th17 cell accumulation.
2026-02-24 | GSE315728 | GEO
Project description:Expression data from intestinal epithelial cells (IECs) [MoGene-1_0-st array]
| PRJNA247394 | ENA