Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide transcriptional profiles of intestinal macrophages from WT and Csf1r-EP4-/- mice during dextran sodium sulfate induced colitis.

ABSTRACT: Genome-wide transcriptional profiles of intestinal macrophages from WT and Csf1r-EP4-/- mice during dextran sodium sulfate induced colitis.

PROVIDER: PRJNA592057 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Genome-wide transcriptional profiles of intestinal macrophages from WT and Csf1r-EP4-/- mice during dextran sodium sulfate induced colitis.

Project description:To define the mechanisms that underlie regeneration driven by EP4+ macrophages, we transcriptionally compared the WT and Csf1r-EP4-/- mature macrophages isolated from colon by 39 days post DSS treatment.

2019-11-28 | GSE141093 | GEO

Dextran sodium sulfate treatment of Pirc rats alters colonic and tumor gene expression

Project description:Dextran sodium sulfate (DSS) causes inflammation in the gut similar to ulcerative colitis in humans. Patients with ulcerative colitis have increased risk of developing colon cancer. We sought to determine whether genes altered in the normal colonic epithelium or tumor differed between sporadic and inflammation-associated tumor development.

2014-01-14 | GSE54035 | GEO

Whole ileal tissue from day 6 Dextran Sodium Sulfate (DSS) administered Il17rafl/fl;Atoh1-cre+/- mice

Project description:Total RNA sequencing (RNA-seq) of the terminal ileum of day 6 Dextran Sodium Sulfate (DSS) administered Il17rafl/fl;Atoh1-cre+ mice and littermate cre- mice was performed.

2022-01-25 | GSE189219 | GEO

Multi-Omics Insights into the Mechanism of Liver Injury in Dextran Sulfate Sodium-Induced Colitis

Project description:Liver injury is a common complication of inflammatory bowel disease (IBD). However, the mechanisms of liver injury development are not clear in IBD patients. Gut microbiota is thought to be engaged in IBD pathogenesis. Here, by an integrated analysis of host transcriptome and colonic microbiome, we have attempted to reveal the mechanism of liver injury in colitis mice. In this study, dextran sulfate sodium (DSS) -induced mice colitis model was constructed. Liver and colon transcriptome results showed that immune response and lipid metabolism-related pathways were dramatically altered, while DNA damage repair-related pathways were only significantly down-regulated in the colon. The microbiota of DSS-treated mice underwent strong transitions. Correlation analyses identified genes associated with liver and colon injury, whose expression was associated with the abundance of liver and gut health-related bacteria Collectively, the results indicate that the liver injury in colitis mice may be related to the intestinal dysbiosis and host-microbiota interactions. These findings may provide new insights for identifying potential targets for the treatment of IBD and its induced liver injury.

2021-08-16 | GSE181959 | GEO

Dextran sodium sulfate treatment of wild type and Pirc rats alters colonic normal tissue gene expression

Project description:Dextran sodium sulfate (DSS) causes inflammation in the gut similar to ulcerative colitis in humans. Patients with ulcerative colitis have increased risk of developing colon cancer. We sought to determine which genes are altered in the normal colonic epithelium, and which changes depend on the Pirc mutation.

2014-01-14 | GSE54005 | GEO

Effect of group X phospholipase A2 deletion in dextran sulfate sodium-induced colitis modeled colon

Project description:Within the secreted phospholipase A2 (sPLA2) family, group X sPLA2 (sPLA2-X) has the highest capacity to hydrolyze cellular membranes and has long been thought to promote inflammation by releasing arachidonic acid (AA), a precursor of pro-inflammatory eicosanoids. Unexpectedly, we found that transgenic mice globally overexpressing human sPLA2-X (PLA2G10-Tg) displayed striking immunosuppressive and lean phenotypes with lymphopenia and increased M2-like macrophages, accompanied by marked elevation of free omega-3 polyunsaturated fatty acids (PUFAs) and their metabolites. Studies using Pla2g10-deficient mice revealed that endogenous sPLA2-X, which is highly expressed in the colon epithelium and spermatozoa, mobilized omega-3 PUFAs or their metabolites to protect against dextran sulfate sodium (DSS)-induced colitis and to promote fertilization, respectively. In colitis, sPLA2-X deficiency increased colorectal expression of Th17 cytokines, and omega-3 PUFAs attenuated their production by lamina propria cells partly through the fatty acid receptor GPR120. In comparison, cytosolic phospholipase A2 (cPLA2alpha) protects from colitis by mobilizing omega-6 AA metabolites including prostaglandin E2. Thus, our results underscore a previously unrecognized role of sPLA2-X as an omega-3 PUFA mobilizer in vivo, segregated mobilization of omega-3 and omega-6 PUFA metabolites by sPLA2-X and cPLA2alpha, respectively, in protection against colitis, and the novel role of a particular sPLA2-X-driven PUFA in fertilization.

2016-02-01 | GSE77144 | GEO

Expansion of Interleukin-22-producing Innate Lymphoid Cells in Tristetraprolindeficient mice protects against Dextran Sulfate Sodium-induced Colitis

Project description:Tristetraprolin (TTP, encoded by Zfp36) is an RNA-binding protein that plays a major role in the control of inflammation. Zfp36 -/-mice spontaneously develop a complex multi-organ inflammatory syndrome that shares many features with spondyloarthritis. Herein, we show that Zfp36 -/-mice are paradoxically protected from Dextran Sulfate Sodium (DSS)-induced colitis. This effect was maintained on a Rag2 -/- background but was lost in Rag2 -/-Il2rg -/-Zfp36 -/-mice that lack innate lymphoid cells (ILCs). Furthermore, we observed a local expansion of type 3 ILCs in the lamina propria of Zfp36 -/-mice. These cells produced large amounts of Interleukin (IL)-22 and were expanded in response to systemic inflammation. Finally, we show that IL-22 contributed to protection of Zfp36 -/-mice against DSSinduced colitis but had a minor impact on their spontaneous inflammatory syndrome. Taken together, these data highlight the complex role of TTP in the control of organ-specific inflammation.

2023-08-01 | GSE236230 | GEO

RNA-Seq of wild type and somatostatin 3 CrispR/Cas9 zebrafish mutants treated with dextran sodium sulfate (DSS)

Project description:Wild type and somatostatin 3 (Sst3) gene CrispR/Cas9 mutants of the AB zebrafish strain were treated with dextran sodium sulfate (DSS) to determine the role of sst3 in the innate immune response.

2020-07-31 | E-MTAB-9018 | biostudies-arrayexpress

Genomic profile of dextran sulphate sodium-induced colitis model in rats

Project description:Background & Aims: Dextran sulphate sodium (DSS) induced colitis in rats is one of the most widely used models of inflammatory bowel disease. Animal models can provide new insights into the pathogenesis of intestinal inflammation, which is still unknown. We have performed a genomic analysis of the DSS rat colitis including an acute and a recovery phase. Methods: Expression profile of 6 control rats were compared with colitic rats at day 1 every other day until day 23 after DSS treatment using the GeneChip Rat Genome 230 2.0 Array (Affymetrix). Functional and pathways analysis were made with the differentially expressed genes. Keywords: Time course and differentially expressed genes analysis

2008-11-01 | GSE9281 | GEO

Colonic gene expression data of acute and chronic dextran sodium sulphate (DSS) colitis mice

Project description:The lack of suitable animal models reflecting chronically relapsing inflammation and tissue remodeling have hindered fibrosis research in inflammatory bowel diseases (IBD). This study investigated changes in connective tissue in a chronic murine model using different cycles of dextran sodium sulphate (DSS) to mimic the relapsing nature of the disease. We used whole gene expression arrays to study differences in colonic gene expression levels between acute and more chronic DSS colitis,

2013-09-03 | GSE42768 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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