Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of GR WT and GR DIM ileum/IEC with DEX, Zn and untreated controls

ABSTRACT: The cytokine TNF drives inflammatory diseases, e.g. Crohn disease. In a mouse model of TNF-induced systemic inflammatory response syndrome (SIRS), severe impact on intestinal epithelial cells (IECs) is observed. Zinc confers complete protection in this model. We found that zinc no longer protects in animals which lack glucocorticoids (GCs), or express mutant versions of their receptor GR in IECs, nor in mice which lack gut microbiota. RNA-seq studies in IECs showed that zinc caused reduction of expression of constitutive (STAT1-induced) interferon-stimulated response (ISRE) genes and Interferon Regulatory Factor (IRF) genes. Since some of these genes are involved in TNF-induced cell death in intestinal crypt Paneth cells, and since zinc has direct effects on the composition of the gut microbiota (such as several Staphylococcus species) and on TNF-induced Paneth cell death, we postulate a new zinc-related anti-inflammatory mechanism. Zinc modulates the gut microbiota, causing less induction of ISRE/IRF genes in crypt cells, less TNF-induced necroptosis in Paneth cells and less fatal evasion of gut bacteria into the system.

ORGANISM(S): Mus musculus

PROVIDER: GSE156242 | GEO | 2020/09/07

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA-seq of WT ileum with DEX, Zn and untreated controls

Project description:The cytokine TNF drives inflammatory diseases, e.g. Crohn disease. In a mouse model of TNF-induced systemic inflammatory response syndrome (SIRS), severe impact on intestinal epithelial cells (IECs) is observed. Zinc confers complete protection in this model. We found that zinc no longer protects in animals which lack glucocorticoids (GCs), or express mutant versions of their receptor GR in IECs, nor in mice which lack gut microbiota. RNA-seq studies in IECs showed that zinc caused reduction of expression of constitutive (STAT1-induced) interferon-stimulated response (ISRE) genes and Interferon Regulatory Factor (IRF) genes. Since some of these genes are involved in TNF-induced cell death in intestinal crypt Paneth cells, and since zinc has direct effects on the composition of the gut microbiota (such as several Staphylococcus species) and on TNF-induced Paneth cell death, we postulate a new zinc-related anti-inflammatory mechanism. Zinc modulates the gut microbiota, causing less induction of ISRE/IRF genes in crypt cells, less TNF-induced necroptosis in Paneth cells and less fatal evasion of gut bacteria into the system.

2020-09-07 | GSE156119 | GEO

RNA-seq of WT liver with DEX, Zn and untreated controls

2020-08-15 | GSE156282 | GEO

IkappaBzeta Controls IL-17-triggered Gene Expression Program in Intestinal Epithelial Cells that Prevents Expansion of SFB and Attenuates Autoimmune Disorders [ATAC-Seq]

Project description:Control of gut microbes is crucial for not only local defense in the intestine but also proper systemic immune responses. Although intestinal epithelial cells (IECs) play important roles in cytokine-mediated control of enterobacteria, the underlying mechanisms are not fully understood. Here we show that deletion of IkappaBzeta in IECs in mice leads to dysbiosis with marked expansion of segmented filamentous bacteria (SFB), thereby enhancing Th17 cell development and exacerbating autoimmune inflammatory diseases. Mechanistically, the IkappaBzeta deficiency results in Paneth cell loss and impaired expression of IL-17-inducible genes involved in IgA production. The Paneth cell loss is caused by aberrant activation of IFN-gamma signaling and a failure of IL-17-mediated recovery from IFN-gamma-induced damage. Thus, the IL-17R–IkappaBzeta axis in IECs contributes to the maintenance of intestinal homeostasis by serving as a key component in a regulatory loop consisting of the gut microbiota and immune cells

2022-12-07 | GSE188253 | GEO

IkappaBzeta Controls IL-17-triggered Gene Expression Program in Intestinal Epithelial Cells that Prevents Expansion of SFB and Attenuates Autoimmune Disorders [ilea]

2022-12-07 | GSE188196 | GEO

IkappaBzeta Controls IL-17-triggered Gene Expression Program in Intestinal Epithelial Cells that Prevents Expansion of SFB and Attenuates Autoimmune Disorders [jejunum]

2022-12-07 | GSE188252 | GEO

transcriptome of purified PC and non-PC fractions: GR-WT & GR-KO

Project description:Paneth Cells (PCs) are secretory cells located in the crypts of Lieberkühn of the small intestine. They produce antimicrobial peptides (AMPs) and are thought to keep the microbiome under control. The cytokine TNF, which functions mainly via its TNF receptor 1 (TNFR1 or P55), is a driving force in many inflammatory bowel disease (IBD) patients, but its impact on PCs is poorly known. We have generated intestinal glucocorticoid receptor knockout mice (GR villin KO) and investigated the diffrences between WT and KO paneth and non-paneth cell fractionf from the cell sorting.

2024-06-17 | GSE269510 | GEO

Reg4+ Deep Crypt Secretory cells function as epithelial niche for Lgr5+ stem cells in colon

Project description:Lgr5+ stem cells reside at crypt bottoms of the small and large intestine. Small intestinal Paneth cells supply Wnt3, EGF and Notch signals to neighboring Lgr5+ stem cells. While the colon lacks Paneth cells, Deep Crypt Secretory (DCS) cells are intermingled with Lgr5+ stem cells at crypt bottoms. Here, we report Reg4 as a marker of DCS cells. To investigate a niche function, we eliminated DCS cells using the diphtheria-toxin receptor gene knocked into the murine Reg4 locus. Ablation of DCS cells results in loss of stem cells from colonic crypts and disrupts gut homeostasis and colon mini-gut formation. In agreement, sorted Reg4+ DCS cells promote organoid formation of single Lgr5+ colon stem cells. Stem cells are forced to generate DCS cells in vitro by combined Notch inhibition and Wnt activation. We conclude that Reg4+ DCS cells serve as Paneth cell equivalents in the colon crypt niche.

2016-10-05 | GSE63256 | GEO

Expression data from mouse crypt

Project description:Paneth cells originate in the stem cell region near the bottom of the gland and release a large number of secretory granules containing antimicrobials. The antimicrobial-rich granules are discharged into the crypt lumen and prevent microbial invasion of the crypt and defend the gland stem cells from microbial damage. We examined the global gene expression profiles in crypt IECs using the Clariom S sDNA array. We analyzed mRNA panels of antimicrobial peptides (AMPs) produced in CSN8ΔIEC and CSN8fl/fl mice.

2018-09-03 | GSE108132 | GEO

Single cell RNA sequencing analysis of germ free (GF) mouse Paneth cells and microbiome-transferred exGF mouse Paneth cells.

Project description:The single cell level Paneth cell transcriptome under gnotobiotic condition has not been resolved. How gut microbiome modulates Paneth cell transcriptome at single cell level in germ-free mice was not known. We used a flow cytometry method to isolate highly pure ileal Paneth cells from germ free (GF) Paneth cell reporter mice (Lyz1-3'UTR-IRES-CreER) and from exGF Paneth cell reporter mice that were transplanted with wild type C57B/l6 mouse gut microbiota (exGF+B6M). These isolated Paneth cells were subjected to single cell RNA sequencing by 10xGenomics.

2023-09-01 | GSE237328 | GEO

Analysis of the role of microbiota in macrophages using single cell RNA sequencing (scRNA-seq).

Project description:Single-cell sequencing of intestinal macrophage was peformed with mice colony stimulating factor 1 receptor promoter (CSF1R) positive cells isolated from the 1/3 distal part of the small intestine of male MaFIA mice at postnatal day 17. Intestinal secretory Paneth cells become differentiated during the first two weeks after birth, which coincides with initial gut microbiota exposure. Their number is significantly reduced in cases of necrotizing enterocolitis (NEC), a deadly disease affecting premature infants. Although known to be associated with intestinal immaturity, its underlying disease mechanisms are unclear. Our analysis of mice treated with antibiotics reveals Paneth cell defects, which promote NEC pathogenesis. Our single cell and genetic analyses demonstrate that gut microbiota induces stem cell differentiation into Paneth cells by controlling the number and heterogeneity of macrophage populations that secrete Wnt ligands. Moreover, differentiated M2 macrophages are able to restore Paneth cell differentiation and rescue NEC-like pathology, while the ablation of Paneth cells is sufficient to induce it, leading to lethality. Our work reveals an unexpected requirement for Paneth cell differentiation through the regulation of gut microbiota-macrophage niches in early postnatal development.

2022-12-16 | GSE141561 | 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