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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]

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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.

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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

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Influenza virus-induced type I interferons disrupt alveolar epithelial repair and tight junction integrity in the developing lung

Project description:Influenza virus-induced type I interferons disrupt alveolar epithelial repair and tight junction integrity in the developing lung

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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.

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Influenza virus-induced type I interferons disrupt alveolar epithelial repair and tight junction integrity in the developing lung

Project description:Type I interferons (IFN-I) are key innate immune mediators which control viral infection in adults. Recently, using a neonatal murine model of influenza A infection (IAV), we demonstrated that IAV-infected murine neonates lacking a functional IFN-I receptor (IFNAR-/-) have significantly improved survival and reduced lung pathology relative to wild-type (WT) neonates. However, the opposite is observed in adults, with IAV-infected IFNAR-/- adults exhibiting enhanced morbidity relative to WT adults, indicating an age-specific IFN-I toxicity in neonates. Therefore, we hypothesized that IAV-induced IFN-I signaling in primary neonatal type II alveolar epithelial cells (TIIECs), the main cell type of IAV infection and initiator of host response in the lung, contributed to age-specific viral pathogenesis. To investigate the role of IFN-I signaling in TIIECs, we performed RNA-Seq on purified TIIECs in a multifactorial design, comparing 1. IFNAR-/- and WT genotypes, 2. neonatal and adult ages, 3. IAV-infected and uninfected, 4. over a three-day time course.Analysis of purified TIIECs revealed age, not infection status, as the primary driver of transcriptional differences in TIIECs. Subsequent pathway analysis demonstrated IAV-infected IFNAR-/- neonates significantly upregulate cell proliferation, tissue repair and tight junction genes at 2-days post-infection (dpi), compared to WT neonates. Next, to determine if these growth and repair differences persisted later in infection, targeted analysis of repair gene expression and immunofluorescent quantification of pulmonary sealing tight junction molecules ZO-1 and occludin was performed at 6-dpi. Relative to WT neonates, IFNAR-/- neonates had significantly higher whole lung occludin staining and repair gene expression. Together, our data demonstrates IFN-I signaling is extremely pathogenic in the developing lung because by disrupting alveolar repair and pulmonary barrier integrity.

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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 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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