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Type 2 inflammation reduces SARS-CoV-2 replication in the airway epithelium in allergic asthma through functional alteration of ciliated epithelial cells II

ABSTRACT: Type 2 inflammation reduces SARS-CoV-2 replication in the airway epithelium in allergic asthma through functional alteration of ciliated epithelial cells II

PROVIDER: PRJNA1062864 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27474988.fastq.gz	Fastqsanger.gz
	SRR27474989.fastq.gz	Fastqsanger.gz
	SRR27474990.fastq.gz	Fastqsanger.gz
	SRR27474991.fastq.gz	Fastqsanger.gz
	SRR27474992.fastq.gz	Fastqsanger.gz

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Type 2 inflammation reduces SARS-CoV-2 replication in the airway epithelium in allergic asthma through functional alteration of ciliated epithelial cells

Project description:Type 2 inflammation reduces SARS-CoV-2 replication in the airway epithelium in allergic asthma through functional alteration of ciliated epithelial cells

| PRJNA1062859 | ENA

Type 2 inflammation reduces SARS-CoV-2 replication in the airway epithelium in allergic asthma through functional alteration of ciliated epithelial cells I

Project description:Type 2 inflammation reduces SARS-CoV-2 replication in the airway epithelium in allergic asthma through functional alteration of ciliated epithelial cells I

| PRJNA1062861 | ENA

Type 2 inflammation reduces SARS-CoV-2 replication in the airway epithelium in allergic asthma through functional alteration of ciliated epithelial cells I

Project description:Despite well-known susceptibilities to other respiratory viral infections, individuals with allergic asthma have shown reduced susceptibility to severe coronavirus disease 2019 (COVID-19).

2024-01-10 | GSE252876 | GEO

Type 2 inflammation reduces SARS-CoV-2 replication in the airway epithelium in allergic asthma through functional alteration of ciliated epithelial cells II

2024-01-10 | GSE252877 | GEO

Type 2 inflammation reduces SARS-CoV-2 replication in the airway epithelium in allergic asthma through functional alteration of ciliated epithelial cells.

Project description:BackgroundDespite well-known susceptibilities to other respiratory viral infections, individuals with allergic asthma have shown reduced susceptibility to severe coronavirus disease 2019 (COVID-19).ObjectiveWe sought to identify mechanisms whereby type 2 inflammation in the airway protects against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) by using bronchial airway epithelial cells (AECs) from aeroallergen-sensitized children with asthma and healthy nonsensitized children.MethodsWe measured SARS-CoV-2 replication and ACE2 protein and performed bulk and single-cell RNA sequencing of ex vivo infected AEC samples with SARS-CoV-2 infection and with or without IL-13 treatment.ResultsWe observed that viral replication was lower in AECs from children with allergic asthma than those from in healthy nonsensitized children and that IL-13 treatment reduced viral replication only in children with allergic asthma and not in healthy children. Lower viral transcript levels were associated with a downregulation of functional pathways of the ciliated epithelium related to differentiation as well as cilia and axoneme production and function, rather than lower ACE2 expression or increases in goblet cells or mucus secretion pathways. Moreover, single-cell RNA sequencing identified specific subsets of relatively undifferentiated ciliated epithelium (which are common in allergic asthma and highly responsive to IL-13) that directly accounted for impaired viral replication.ConclusionOur results identify a novel mechanism of innate protection against SARS-CoV-2 in allergic asthma that provides important molecular and clinical insights during the ongoing COVID-19 pandemic.

| S-EPMC10052850 | biostudies-literature

Targeting mitochondrial reactive oxygen species alleviates allergic airway disease in a mouse model of obese allergic asthma

Project description:Obesity is associated with severe, difficult to control asthma, and increased airway oxidative stress. Mitochondrial reactive oxygen species (mROS) are an important source of oxidative stress leading us to hypothesize that targeting mROS in obese allergic asthma might be an effective treatment strategy. Using a mouse model of house dust mite (HDM) induced allergic airway disease in mice fed a low- (LFD) or high-fat diet (HFD), and the mitochondrial antioxidant MitoQuinone (MitoQ); we investigated the effects of obesity and mROS on airway inflammation, remodelling and airway hyperreactivity (AHR). HDM induces airway inflammation, remodelling and hyperreactivity in both lean and obese mice. Obese allergic mice showed increased lung tissue eotaxin levels, airway tissue eosinophilia and AHR when compared to lean allergic mice. MitoQ reduced markers of airway inflammation, remodelling and hyperreactivity in both lean and obese allergic mice, and tissue eosinophilia in obeseHDM mice. mROS regulates cell signalling by protein oxidation of multiple downstream targets: MitoQ reduced HDM-induced cysteine-sulfenylation of several proteins including those involved in the unfolded protein response (UPR). In summary, mROS mediates the development of allergic airway disease and hence MitoQ might be effective for the treatment for asthma, and specific features of obese asthma.

2023-06-02 | PXD029715 | Pride

Type 2 inflammation reduces SARS-CoV-2 replication in the airway epithelium in allergic asthma through functional alteration of ciliated epithelial cells

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

2024-01-10 | GSE252878 | GEO

Endotype of Allergic Asthma with Airway Obstruction in Urban Children

Project description:In the first decade of life, high-asthma risk urban children develop stable phenotypes of respiratory health versus disease that link early life environmental exposures to childhood allergic sensitization and asthma. Moreover, unique patterns of nasal gene expression demonstrate how specific molecular pathways underlie distinct respiratory phenotypes, including allergic and non-allergic asthma.

2021-04-01 | GSE145505 | GEO

IL-22 inhibits allergic airway inflammation in house dust mite-induced asthma models

Project description:While the pathogenesis of asthma is mainly orchestrated by antigen-specific Th2 cells and their cytokines, recent findings indicate the involvement of other subsets of helper T cells including Th17 cells. Previous studies have shown that IL-22, one of Th17 cell-related cytokines, plays multiple roles in regulating allergic airway inflammation; however, the mechanism underlying the Il-22-mediated regulation remains unclear. Here, we show that allergic airway inflammation upon intratracheal administration of house dust mite extract (HDM), a representative allergen, were exacerbated in IL-22-deficient mice. To address the molecular mechanisms by which IL-22 inhibits the development of HDM-induced allergic airway inflammation, we next performed an unbiased comprehensive screening of genes induced by IL-22 administration in the lung by RNA-seq analysis.

2017-08-10 | GSE100858 | GEO

The Ciliated Cell Transcriptome: Ciliated Mouse Tracheal Epithelial Cells vs Control Non-ciliated Mouse Tracheal Epithelial Cells during in Vitro Differentiation

Project description:Transcriptional profiling of ciliating mouse tracheal epithelial cells compared to non-ciliating cells at two timepoints, ALI+4 and ALI+12, during differentiation in vitro. These cells are obtained from a transgenic mouse expressing GFP from a human FOXJ1 promoter, so that cells destined to become ciliated can be sorted by FACS based on their expression of GFP. Likewise, the control non-ciliated cells are identified by their lack of GFP expression. Ciliated cells were compared to Universal Reference RNA, and non-ciliated cells were compared to Universal Reference RNA. Two-color arrays were used to compare non-ciliated cells, or ciliated cell samples taken at 4 days or 12 days after establishment of the air-liquid interface (ALI), to a Universal Reference RNA. Ciliated cells vs. Universal Reference RNA or Non-ciliated cells vs. Universal Reference RNA. 3 biological replicates from independently grown and harvested cell cultures were performed for non-ciliated cells, 5 biological replicates were performed for a ciliated cell samples at ALI+12, and 3 biological replicates plus 2 technical replicates were performed for ciliated cell samples at ALI+4.

2012-11-29 | E-GEOD-42500 | biostudies-arrayexpress

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