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Interferons disrupt lung epithelial repair during recovery from respiratory infection

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE148712 | GEO | 2020/06/12

REPOSITORIES: GEO

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

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 | GSE148709 | GEO

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

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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).

| S-EPMC7292500 | biostudies-literature

Interferons disrupt lung epithelial repair during recovery from respiratory infection

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

| PRJNA625478 | ENA

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

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

| PRJNA625462 | ENA

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

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

| PRJNA625463 | ENA

Type III interferons disrupt the lung epithelial barrier upon viral recognition.

Project description:Lower respiratory tract viral infections are a leading cause of mortality. Mounting evidence indicates that most severe cases are characterized by aberrant immune responses and do not depend on viral burden. Here, we assessed how type III interferons (IFN-?) contribute to the pathogenesis induced by RNA viruses. We report IFN-? is present in the lower, but not upper, airways of COVID-19 patients. In mice, we demonstrate IFN-? produced by lung dendritic cells in response to a synthetic viral RNA induces barrier damage, causing susceptibility to lethal bacterial superinfections. These findings provide a strong rationale for rethinking the pathophysiological role of IFN-? and its possible use in the clinical practice against endemic viruses, such as influenza virus, as well as the emerging SARS-CoV-2 viral infection.

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Type I interferons link viral infection to enhanced epithelial turnover and repair.

Project description:The host immune system functions constantly to maintain chronic commensal and pathogenic organisms in check. The consequences of these immune responses on host physiology are as yet unexplored, and may have long-term implications in health and disease. We show that chronic viral infection increases epithelial turnover in multiple tissues, and the antiviral cytokines type I interferons (IFNs) mediate this response. Using a murine model with persistently elevated type I IFNs in the absence of exogenous viral infection, the Irgm1(-/-) mouse, we demonstrate that type I IFNs act through nonepithelial cells, including macrophages, to promote increased epithelial turnover and wound repair. Downstream of type I IFN signaling, the highly related IFN-stimulated genes Apolipoprotein L9a and b activate epithelial proliferation through ERK activation. Our findings demonstrate that the host immune response to chronic viral infection has systemic effects on epithelial turnover through a myeloid-epithelial circuit.

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Epigenetic and Transcriptomic Regulation of Lung Repair during Recovery from Influenza Infection.

Project description:Seasonal and pandemic influenza is a cause of morbidity and mortality worldwide. Most people infected with influenza virus display mild-to-moderate disease phenotypes and recover within a few weeks. Influenza is known to cause persistent alveolitis in animal models; however, little is known about the molecular pathways involved in this phenotype. We challenged C57BL/6 mice with influenza A/PR/8/34 and examined lung pathologic processes and inflammation, as well as transcriptomic and epigenetic changes at 21 to 60 days after infection. Influenza induced persistent parenchymal lung inflammation, alveolar epithelial metaplasia, and epithelial endoplasmic reticulum stress that were evident after the clearance of virus and resolution of morbidity. Influenza infection induced robust changes in the lung transcriptome, including a significant impact on inflammatory and extracellular matrix protein expression. Despite the robust changes in lung gene expression, preceding influenza (21 days) did not exacerbate secondary Staphylococcus aureus infection. Finally, we examined the impact of influenza on miRNA expression in the lung and found an increase in miR-155. miR-155 knockout mice recovered from influenza infection faster than controls and had decreased lung inflammation and endoplasmic reticulum stress. These data illuminate the dynamic molecular changes in the lung in the weeks after influenza infection and characterize the repair process, identifying a novel role for miR-155.

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Myeloid and epithelial-derived RELM contribute to tissue repair following lung helminth infection

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

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