Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Circadian control of duodenal regulatory T cells by enteric neurons and eosinophils

ABSTRACT: Multiple intestinal functions including nutrient absorption and peristalsis display regional specialization as well as time-of-day effect under the control of circadian rhythm. We investigated the role of these adaptations on intestinal immune system and response to dietary antigens. We found that oral challenge during the night resulted in more protective tolerance, which correlated with nocturnal expansion of regulatory T (Treg) cells in proximal small intestine lamina propria. Expansion of Treg cells was supported by eosinophils and clock gene-dependent rhythmic production of follistatin by enteric neurons. Circadian entrainment of these changes depended on light exposure and locomotor activity but not the time of food intake. These data suggest that circadian and regional adaptations in the intestine limit the severity of allergic reactions during the active phase.

ORGANISM(S): Mus musculus

PROVIDER: GSE246542 | GEO | 2024/07/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA-seq in Prdm16 KO duodenal crypts

Project description:The adult intestinal epithelium is maintained by a continuous replacement of differentiated cells from stem cells. Previous studies suggest that cellular metabolic pathways regulate intestinal stem cell activity and differentiation. However, little is known about the cell-intrinsic factors that control these metabolic programs. Here, we identify the transcription factor PRDM16 as a critical regulator of intestinal metabolic programing and stem cell differentiation. Acute deletion of Prdm16 in adult mice causes severe intestinal wasting, apoptosis, and an accumulation of poorly differentiated cells in the crypt. Prdm16-deficient crypts display decreased expression levels of fatty acid oxidation (FAO) genes and reduced rates of FAO. PRDM16 binds, along with its protein partners PPARγ and PPARα, to the promoter and enhancer regions of many FAO genes. The loss of Prdm16 or inhibition of FAO impaired the transition of intestinal stem cells into transit amplifying cells. Notably, PRDM16 expression is highest in the duodenum and declines distally along the intestine. This gradient of PRDM16 expression controls the region-specific expression of the FAO program and underlies the differential reliance of region-specific stem cells on FAO. Altogether, this study establishes PRDM16 as a regional-specific regulator of metabolism and stem cell differentiation in the intestine.

2020-02-26 | GSE121009 | GEO

H3K27Ac ChIP-Seq in Prdm16 KO duodenal crypts

Project description:The adult intestinal epithelium is maintained by a continuous replacement of differentiated cells from stem cells. Previous studies suggest that cellular metabolic pathways regulate intestinal stem cell activity and differentiation. However, little is known about the cell-intrinsic factors that control these metabolic programs. Here, we identify the transcription factor PRDM16 as a critical regulator of intestinal metabolic programing and stem cell differentiation. Acute deletion of Prdm16 in adult mice causes severe intestinal wasting, apoptosis, and an accumulation of poorly differentiated cells in the crypt. Prdm16-deficient crypts display decreased expression levels of fatty acid oxidation (FAO) genes and reduced rates of FAO. PRDM16 binds, along with its protein partners PPAR? and PPAR?, to the promoter and enhancer regions of many FAO genes. The loss of Prdm16 or inhibition of FAO impaired the transition of intestinal stem cells into transit amplifying cells. Notably, PRDM16 expression is highest in the duodenum and declines distally along the intestine. This gradient of PRDM16 expression controls the region-specific expression of the FAO program and underlies the differential reliance of region-specific stem cells on FAO. Altogether, this study establishes PRDM16 as a regional-specific regulator of metabolism and stem cell differentiation in the intestine.

2020-02-26 | GSE120897 | GEO

Expression data from human Duodenal Organ Chips

Project description:Environmental Enteric Dysfunction (EED) is a chronic inflammatory condition of the intestine characterized by villus blunting, compromised intestinal barrier function, and reduced nutrient absorption. Here, we show that key genotypic and phenotypic features of EED-associated intestinal injury can be reconstituted in a human intestine-on-a-chip (Intestine Chip) microfluidic culture device lined by organoid-derived intestinal epithelial cells from EED patients and cultured in nutrient deficient medium lacking niacinamide and tryptophan (-N/-T). Exposure of EED Intestine Chips to -N/-T deficiencies resulted in transcriptional changes similar to those seen in clinical EED patient samples including congruent changes in six of the top ten upregulated genes. Exposure of EED Intestine Chips or chips lined by healthy intestinal epithelium (healthy Intestine Chips) to -N/-T medium resulted in severe villus blunting and barrier dysfunction, as well as impairment of fatty acid uptake and amino acid transport.

2022-05-06 | GSE202282 | GEO

Generation of transcriptional regulatory network of Lgr5+ small and large intestinal stem cells from mouse [ATAC-seq]

Project description:The goal of this study is to survey transcriptional machinery in intestinal stem cells from small and large intestine of mice. We established intestinal stem cell specific gene-regulatroy network to understand regional identity.

2023-04-20 | GSE196913 | GEO

Generation of transcriptional regulatory network of Lgr5+ small and large intestinal stem cells from mouse [scRNA-seq]

2023-04-20 | GSE196915 | GEO

Generation of transcriptional regulatory network of Lgr5+ small and large intestinal stem cells from mouse [RNA-seq]

2023-04-20 | GSE196914 | GEO

c-Maf-dependent Treg cell control of intestinal TH17 cells and IgA establishes host–microbiota homeostasis

Project description:Foxp3+ regulatory T (Treg) cells are essential for immunological tolerance and homeostasis. In peripheral tissues, Treg cells acquire enhanced suppressive functions and co-opt distinct transcriptional modules, allowing context and tissue-dependent immune regulation. Here we show that the transcription factor c-Maf was highly expressed by effector Treg cells and controlled their IL-10 production. In the intestine, c-Maf was required for the differentiation of RORgt+ microbiota-dependent Treg cells, and restricted their production of inflammatory cytokines. Consequently, Treg cell-specific loss of c-Maf resulted in perturbed intestinal homeostasis, microbial dysbiosis and a selective failure to control Th17 responses during homeostasis and upon chemically induced epithelial damage. Molecular profiling revealed that c-Maf regulated expression of key genes of the transcriptional signature of intestinal Treg cells, including Rorc and Il10. Thus, our study identifies a key role of c-Maf in preserving the identity and function of intestinal Treg cells, essential for the control of intestinal immune homeostasis.

2018-12-18 | GSE106396 | GEO

Project description:Nocturnal habitat intestinal flora

| PRJNA912996 | ENA

Composition of colonic microbes in mice deficient in intestinal Treg subsets

Project description:Regulatory T cells (Tregs) are immune cells that play a crucial role in maintaining tolerance to harmless antigens, including commensal microbes. In the intestine, Tregs can be classified into subsets based on their expression of transcription factors Helios, Rorg, Gata3 and cMaf. The exact functions of the intestinal Treg subsets and their role in maintaining tolerance to intestinal microbes is not fully understood. Here, we generated conditional knockout mice of each Treg subset and profiled the composition of their intestinal microbiota by performing 16S rRNA sequencing of stool from conditional knockouts and matched littermate controls.

2023-12-20 | GSE241887 | GEO

Regionally defined stem cell growth directs cell fate during intestinal nutrient adaptation

Project description:The adult intestine is a regionalized organ, whose size and cellular composition is adjusted in response to nutrient status. This involves dynamic regulation of intestinal stem cell (ISC) proliferation and differentiation. How nutrient signaling integrates with mechanisms controlling cell fate to achieve regional changes in intestinal cell composition remains unclear. Here we show that nutrient adaptation involves highly region-specific control of intestinal cell size, number and differentiation. Our data uncovered a mechanism by which mTOR complex 1 activation increases ISC size in a region-specific manner. This promotes Delta expression to direct cell fate towards the absorptive enteroblast lineage, while inhibiting secretory enteroendocrine cell differentiation. Thus, ISC size acts as an early fate determinant allowing regional control of intestinal cell differentiation in response to nutrition.

2024-02-14 | GSE222254 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data