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Interferons disrupt lung epithelial repair during recovery from respiratory infection

ABSTRACT: Interferons disrupt lung epithelial repair during recovery from respiratory infection

PROVIDER: PRJNA625478 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11548540.fastq.gz	Fastqsanger.gz
	SRR11548541.fastq.gz	Fastqsanger.gz
	SRR11548542.fastq.gz	Fastqsanger.gz
	SRR11548543.fastq.gz	Fastqsanger.gz
	SRR11548544.fastq.gz	Fastqsanger.gz

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

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

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

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

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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

Interferons disrupt lung epithelial repair during recovery from respiratory infection

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-06-12 | GSE148712 | GEO

Type I and III interferons disrupt lung epithelial repair during recovery from viral infection.

Project description:Excessive cytokine signaling frequently exacerbates lung tissue damage during respiratory viral infection. Type I (IFN-? and IFN-?) and III (IFN-?) interferons are host-produced antiviral cytokines. Prolonged IFN-? and IFN-? responses can lead to harmful proinflammatory effects, whereas IFN-? mainly signals in epithelia, thereby inducing localized antiviral immunity. In this work, we show that IFN signaling interferes with lung repair during influenza recovery in mice, with IFN-? driving these effects most potently. IFN-induced protein p53 directly reduces epithelial proliferation and differentiation, which increases disease severity and susceptibility to bacterial superinfections. Thus, excessive or prolonged IFN production aggravates viral infection by impairing lung epithelial regeneration. Timing and duration are therefore critical parameters of endogenous IFN action and should be considered carefully for IFN therapeutic strategies against viral infections such as influenza and coronavirus disease 2019 (COVID-19).

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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.

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DNA repair and recovery of RNA synthesis following exposure to ultraviolet light are delayed in long genes

Project description:The kinetics of DNA repair and RNA synthesis recovery in human cells following UV-irradiation were assessed using nascent RNA Bru-seq and quantitative long PCR. It was found that UV light inhibited transcription elongation and that recovery of RNA synthesis occurred as a wave in the 5’-3’ direction with slow recovery and TC-NER at the 3’ end of long genes. RNA synthesis resumed fully at the 3’-end of genes after a 24-hour recovery in wild-type fibroblasts, but not in cells deficient in transcription-coupled nucleotide excision repair (TC-NER) or global genomic NER (GG-NER). Different transcription recovery profiles were found for individual genes but these differences did not fully correlate to differences in DNA repair of these genes. Our study gives the first genome-wide view of how UV-induced lesions affect transcription and how the recovery of RNA synthesis of large genes are particularly delayed by the apparent lack of resumption of transcription by arrested polymerases. This study is composed of three identical experiments run in three different cell lines. For each experiment, there is one control (mock irradiated cells) and four test samples (0h, 2h, 6h and 24h after UV 10J irradiation).

2015-03-03 | E-GEOD-65985 | biostudies-arrayexpress

Eutherian interferons

Project description:Eutherian interferons

| PRJEB36709 | ENA