Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Type III interferons induce pyroptosis in gut epithelial cells and delay tissue restitution upon intestinal injury

ABSTRACT: To investigate the transcriptional program within the intestinal epithelial cells (IECs) controlling the impact of type III interferons (IFN-λ) on intestinal recovery, we performed a single-cell RNA sequencing (scRNA-seq) on murine IECs following irradiation.

ORGANISM(S): Mus musculus

PROVIDER: GSE246333 | GEO | 2024/12/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Type III interferons induce pyroptosis in gut epithelial cells and delay tissue restitution upon acute intestinal injury.

Project description:To determine the transcriptional programs initiated by IFN-λ to delay tissue restitution, we isolated intestinal crypts from the small intestine of VilCREIfnlr1fl/fl mice or WT littermates that have been irradiated and performed targeted transcriptomics analysis

2024-04-01 | GSE247149 | GEO

Type III interferons induce pyroptosis in gut epithelial cells and delay tissue restitution upon intestinal injury

Project description:Type III interferons induce pyroptosis in gut epithelial cells and delay tissue restitution upon intestinal injury

| PRJNA1032569 | ENA

Type III interferons induce pyroptosis in gut epithelial cells and impair tissue repair upon intestinal injury.

Project description:Tissue damage and repair are hallmarks of inflammation. Despite a wealth of information on the mechanisms that govern tissue damage, mechanistic insight on how inflammation affects repair is lacking. Here, we investigated how interferons influence tissue repair after damage to the intestinal mucosa. We found that type III, not type I or II, interferons delay epithelial cell regeneration by inducing the upregulation of Z-DNA-binding protein 1 (ZBP1). Z-nucleic acids formed following intestinal damage are sensed by ZBP1, leading to Caspase-8 activation, and cleavage of Gasdermin C (GSDMC). Cleaved GSDMC drives epithelial cell death by pyroptosis and delays repair of the large or small intestine after colitis or irradiation, respectively. The type III interferon/ZBP1/Caspase-8/GSDMC axis is also active in patients with inflammatory bowel disease (IBD). Our findings highlight the capacity of type III interferons to delay gut repair, which has important implications for IBD patients or individuals exposed to radiation therapies.

2024-11-01 | GSE277150 | GEO

Type III interferons induce pyroptosis in gut epithelial cells and impair tissue repair upon intestinal injury.

Project description:Tissue damage and repair are hallmarks of the inflammatory process. Despite a wealth of information on the mechanisms that govern tissue damage, mechanistic insight on how inflammatory mediators affect repair is lacking. Here, we investigated how interferons influence tissue repair after damage to the intestinal mucosa driven by inflammation or genotoxicity. We found that type III, but not type I or II, interferons delay epithelial cell regeneration by inducing the upregulation of Z-DNA-binding protein 1 (ZBP1). Z-nucleic acids formed during the damage and repair process are then sensed by ZBP-1, leading to Caspase-8 activation, and cleavage of Gasdermin C (GSDMC). Cleaved GSDMC drives epithelial cell death by pyroptosis and delays the re-epithelialization of the large or small intestine after colitis or irradiation, respectively. We also found that the type III interferon/ZBP1/Caspase-8/GSDMC pathway is activated in patients with inflammatory bowel disease (IBD). Our findings highlight a molecular signaling cascade initiated by type III interferons that delays intestinal tissue repair, which has important implications for IBD patients or individuals exposed to radiation therapies.

2024-11-01 | GSE276837 | GEO

Type III interferons induce pyroptosis in gut epithelial cells and delay tissue restitution upon acute intestinal injury.

Project description:Type III interferons induce pyroptosis in gut epithelial cells and delay tissue restitution upon acute intestinal injury.

| PRJNA1036441 | ENA

Transcriptional response of intestinal epithelial cells to type I and III IFN

Project description:RNAseq of intestinal epithelial cell (IEC) organoids and treated with PBS, interferon beta (IFNB), or interferon lambda (IFNL). RNAseq of IECs sorted from neonatal mouse intestines following treatment with PBS, IFNB, or IFNL.

2019-12-18 | GSE142166 | GEO

Type III interferons induce pyroptosis in gut epithelial cells and impair tissue repair upon intestinal injury.

Project description:Type III interferons induce pyroptosis in gut epithelial cells and impair tissue repair upon intestinal injury.

| PRJNA1160875 | ENA

Type III interferons induce pyroptosis in gut epithelial cells and impair tissue repair upon intestinal injury.

Project description:Type III interferons induce pyroptosis in gut epithelial cells and impair tissue repair upon intestinal injury.

| PRJNA1159204 | ENA

Interferons disrupt lung epithelial repair during recovery from respiratory infection [RN200717]

Project description:Respiratory viral infections cause lung epithelial damage, barrier dysfunction and severe disease. Type I interferons (IFN-a/b) are antiviral cytokines whose therapeutic use is limited by well-characterized pleiotropic effects. Type III IFNs (IFN-λ) are less pro-inflammatory and regarded a superior treatment option. Here, we show that IFN signalling reduces lung epithelial proliferation and differentiation and increases epithelial apoptosis during recovery from viral infection. This delays epithelial repair, increasing disease severity and the risk of bacterial superinfection. IFN-a has least effects, with IFN-b intermediate and IFN-λ strongest action.

2020-06-12 | GSE148710 | GEO

Interferons disrupt lung epithelial repair during recovery from respiratory infection [RN19197]

2020-06-12 | GSE148709 | GEO