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IL-13 decreases suceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo [Bulk RNA-seq]

ABSTRACT: IL-13 decreases suceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo [Bulk RNA-seq]

PROVIDER: PRJNA1048482 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27046366_1.fastq.gz	Fastqsanger.gz
	SRR27046366_2.fastq.gz	Fastqsanger.gz
	SRR27046367_1.fastq.gz	Fastqsanger.gz
	SRR27046367_2.fastq.gz	Fastqsanger.gz
	SRR27046368_1.fastq.gz	Fastqsanger.gz

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IL-13 decreases suceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo

Project description:IL-13 decreases suceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo

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IL-13 decreases suceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo [scRNA-seq]

Project description:IL-13 decreases suceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo [scRNA-seq]

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IL-13 decreases suceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo [scRNA-seq]

Project description:Human airway epithelia (HAE) undergo inflammation-induced remodeling in chronic lung diseases such as asthma and chronic bronchitis. The role of type 2 inflammation-induced epithelial remodeling in SARS-CoV-2 infection and the course of COVID-19 is unclear, moreover, there is discrepancy in the literature regarding the potential benefit of treatments that modulate type 2 inflammation. We investigated the role of IL-13-induced inflammation on SARS-CoV-2 binding/entry, replication, and host response in primary HAE cells in vitro and in a model of mouse-adapted SARS-CoV-2 in vivo. IL-13 protected airway epithelial cells from SARS-CoV-2 infection in vitro by decreasing the abundance of ACE2- expressing ciliated cells rather than by neutralization in the airway surface liquid or by interferon-mediated antiviral effects. In contrast, IL-13 worsened the severity of disease in mice in vivo; the effects were mediated by eicosanoid signaling and were abolished in mice deficient in the phospholipase A2 enzyme PLA2G2D. We conclude that IL-13-induced inflammation affects multiple steps of SARS-CoV-2-induced disease pathogenesis. Whereas IL-13-induced inflammation may be protective against initial infection at the airway epithelium, it enhances disease severity once infection progresses in vivo; blockade of IL-13 and/or eicosanoid signaling may be protective against progression to severe lung disease.

2025-06-30 | GSE249307 | GEO

IL-13 decreases suceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo [Bulk RNA-seq]

2024-06-26 | GSE249304 | GEO

IL-13 decreases suceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo

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

2024-06-28 | GSE249308 | GEO

IL-13 decreases susceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo.

Project description:Treatments available to prevent progression of virus-induced lung diseases, including coronavirus disease 2019 (COVID-19) are of limited benefit once respiratory failure occurs. The efficacy of approved and emerging cytokine signaling-modulating antibodies is variable and is affected by disease course and patient-specific inflammation patterns. Therefore, understanding the role of inflammation on the viral infectious cycle is critical for effective use of cytokine-modulating agents. We investigated the role of the type 2 cytokine IL-13 on SARS-CoV-2 binding/entry, replication, and host response in primary HAE cells in vitro and in a model of mouse-adapted SARS-CoV-2 infection in vivo. IL-13 protected airway epithelial cells from SARS-CoV-2 infection in vitro by decreasing the abundance of ACE2-expressing ciliated cells rather than by neutralization in the airway surface liquid or by interferon-mediated antiviral effects. In contrast, IL-13 worsened disease severity in mice; the effects were mediated by eicosanoid signaling and were abolished in mice deficient in the phospholipase A2 enzyme PLA2G2D. We conclude that IL-13-induced inflammation differentially affects multiple steps of COVID-19 pathogenesis. IL-13-induced inflammation may be protective against initial SARS-CoV-2 airway epithelial infection; however, it enhances disease progression in vivo. Blockade of IL-13 and/or eicosanoid signaling may be protective against progression to severe respiratory virus-induced lung disease.

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Project description:COVID-19 Suceptibility Florida

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3D Culture of human lung fibroblasts decreases proliferative and increases extracellular matrix remodeling genes

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Reduction of ZFX levels decreases histone H4 acetylation and increases Pol2 pausing at target promoters

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COVID-19 Suceptibility Florida

Project description:To reveal genetic determinants of susceptibility to COVID-19 severity in the population and further explore potential immune-related factors, we performed a genome-wide association study on 284 confirmed COVID-19 patients (cases) and 95 healthy individuals (controls). We compared cases and controls of European (EUR) ancestry and African American (AFR) ancestry separately. To further exploring the linkage between HLA and COVID-19 severity, we applied fine-mapping analysis to dissect the HLA association with mild and severe cases.

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