Transcriptomic analysis in airway epithelial cells in HDM-sensitized mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA786791 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17155415.fastq.gz | Fastqsanger.gz | |||
| SRR17155416.fastq.gz | Fastqsanger.gz | |||
| SRR17155417.fastq.gz | Fastqsanger.gz | |||
| SRR17155418.fastq.gz | Fastqsanger.gz | |||
| SRR17155439.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:Purpose: To elucidate the roles of airway epithelial STAT3 in allergic airway inflammation. Method: Doxycycline-induced airway epithelial cells-specific STAT3-deficient mice (STAT3-cKO) and their genetic control mice (STAT3-WT) were sensitized intratracheally twice with house dust mite (HDM) extract or PBS at a 7-day interval. Airway epithelial cells were isolated by a cell sorter 48 h after the last senstization. N=2 each. Results: Using an optimized data analysis workflow, 206 transcripts showed differential expression between HDM-treated STAT3-WT and STAT3-cKO with adjusted p value <0.05.
2022-04-01 | GSE190345 | GEO
Project description:Purpose: To elucidate the effects of SCD1 inhibitor in allergic airway inflammation. Method: Wild-type mice were sensitized intratracheally twice with house dust mite (HDM) extract at a 7-day interval. Along with that, an SCD-1 inhibitor, A939572 was also administered intraperitoneally daily. Airway epithelial cells were isolated by a cell sorter 48 h after the last senstization. N=2 each. Results: Using an optimized data analysis workflow, 385 transcripts showed differential expression between SCD1 inhibitor-treated mice and DMSO (vehicle)-treated mice with adjusted p value <0.05.
2022-04-01 | GSE190343 | GEO
Project description:Transcriptomic analysis in airway epithelial cells in HDM-sensitized STAT3-WT and STAT3-cKO mice
| PRJNA786787 | ENA
Project description:Transcriptomic analysis in airway epithelial cells in HDM-sensitized and SCD1 inhibitor-treated or vehicle-treated mice
| PRJNA786789 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-04-01 | GSE190346 | GEO
Project description:The aim of this study was to investigate differential expression in a house dust mite (HDM) exposure model of asthma in rhesus macaques. HDM sensitization was performed by subcutaneous injection of HDM followed by intranasal HDM for 2-3 hours twice a week. Animals were mock-sensitized (PBS) or sensitized to HDM antigen. Gene expression was measured in lung biopsies before and fifteen weeks after treatment.
2011-11-30 | E-GEOD-23327 | biostudies-arrayexpress
Project description:Background: A specific subset of regulatory IL-10 producing B cells has been extensively studied in autoimmune and inflammatory pathologies. These cells are able to constrain exacerbated inflammation by inhibiting T cell mediated responses and maturation of antigen presenting cells. In allergic diseases, observations that increase of regulatory B cells is necessary for allergen tolerance suggest that development of allergic asthma would be associated with a defect in the regulatory B cells compartment. Objective: We sought to (i) characterize regulatory IL-10+ regulatory B cell subset in Balb/c mice by microarray and flow cytometry and (ii) investigate their regulatory capacity in vivo in a house dust mite model of allergic asthma. Results: We identified an IL-10 producing B cells subset able to control T cell proliferation in vitro in both control and asthmatic mice. This subset is decreased in allergic mice. IL-10+ Breg cells express high levels of CD9 and upregulate CD70 and CD73 after activation. Expression of CD9 allows identifying more than 50% of Bregs. Interestingly CD9+ B cells inhibit TH2-TH17 allergic airway inflammation in vivo after adoptive transfer in an IL-10 dependent manner. Conclusions: Herein, we demonstrate that induction of allergic asthma dampens the generation of Bregs contributing to exacerbated airway inflammation. We identified a distinct CD9+ Breg-cell population decreased in lung of HDM mice and able to control asthma and allergic airway inflammation by producing IL-10 after adoptive transfer. This study points B cells as an interesting therapeutic target in allergic asthma. IL-10+ B cells (n=3) and 3 IL-10- B cells (n=3) in control mice + IL-10+ B cells (n=3) and 3 IL-10- B cells (n=3) from asthmatic allergic (HDM) mice
2015-03-01 | E-GEOD-57772 | biostudies-arrayexpress
Project description:Airway macrophages (AMs) are the most abundant leukocytes in the healthy airway lumen and have a highly specialised but plastic phenotype that is governed by the local microenvironment. AMs are thought to maintain immunological homeostasis in the steady state, but have also been implicated in the pathogenesis of allergic airway disease (AAD). To better understand these potentially contrasting AM functions, bulk RNA sequencing was performed on murine AMs obtained during experimental AAD driven by repeated house dust mite inhalation (AM[HDM]s), comparing to control AMs from non-allergic mice. AM[HDM]s showed increased expression of genes associated with antigen presentation, inflammatory cell recruitment and tissue repair, including several chemokines and matrix metalloproteinases. This was accompanied by increased expression of mitochondrial electron transport chain subunit genes and the retinoic acid biosynthetic enzyme gene Raldh2. Conversely, AM[HDM]s displayed decreased expression of a number of cell cycle genes, genes related to cytoskeletal functions and a subset of genes implicated in antimicrobial innate immunity, such as Tlr5, Il18 and Tnf. Differential gene expression in AM[HDM]s was consistent with upstream effects of the cytokines IL-4 and IFN-γ, both of which were at increased concentrations in lung tissue after HDM treatment. These data highlight diverse gene expression changes in the total AM population in a clinically relevant mouse model of AAD, overall suggestive of contributions to inflammation and tissue repair/remodelling, but decreases in certain steady state cellular and immunological functions.
2020-05-20 | GSE148590 | GEO
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
Project description:Levels of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, are increased in lung, sputum, exhaled breath condensate and plasma samples from asthma patients. ADMA is metabolized primarily by dimethylarginine dimethylaminohydrolase 1 (DDAH1) and DDAH2. We determined the effect of DDAH1 overexpression on development of allergic inflammation in mouse models of asthma. Wild type and DDAH1-transgenic mice were challenged with PBS or house dust mite (HDM). Airway inflammation was assessed by bronchoalveolar lavage (BAL) total and differential cell counts. Gene expression in lungs was determined by RNA-Seq and RT-quantitative PCR (qPCR). The expression of DDAH1 and DDAH2 was decreased in the lungs of mice following HDM exposure. Transgenic overexpression of DDAH1 resulted in decreased BAL total cell and eosinophil numbers following HDM exposure. Total IgE levels in serum and BAL fluid were decreased in HDM-exposed DDAH1-transgenic mice compared to HDM-exposed wild type mice. RNA-Seq results showed downregulation of genes in inducible nitric oxide synthase (iNOS) signaling pathway in PBS-treated DDAH1 transgenic mice versus PBS-treated wild type mice and downregulation of genes in IL-13/FOXA2 signaling pathway in HDM-treated DDAH1 transgenic mice versus HDM-treated wild type mice. Our findings suggest that decreased expression of DDAH1 in airway epithelial cells may contribute to allergic asthma and overexpression of DDAH1 attenuates allergen-induced airway inflammation through modulation of Th2 responses. mRNA profiles of WT and DDAH1-transgenic mice treated with PBS or house dust mite (HDM).
2013-12-03 | E-GEOD-49047 | biostudies-arrayexpress