Transcriptomics analysis of aged asthmatic lung and treated with dexamethasone during HDM induced airway inflammaton
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ABSTRACT:
PROVIDER: PRJNA740315 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14891955_1.fastq.gz | Fastqsanger.gz | |||
| SRR14891955_2.fastq.gz | Fastqsanger.gz | |||
| SRR14891956_1.fastq.gz | Fastqsanger.gz | |||
| SRR14891956_2.fastq.gz | Fastqsanger.gz | |||
| SRR14891957_1.fastq.gz | Fastqsanger.gz |
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Project description:This study was designed to evaluate the lung transcriptome analysis against dexamethasone treatment throughout HDM challenge period in the aged (80-82 Weeks) mice. The lung samples from aged inflammed mice with or without dexamethasone treatmrnt were isolated followed by RNA isolation and RNA sequence analysis.
2021-06-24 | GSE178770 | GEO
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:The goal of the was to evaluate the mRNA expression profile of non-asthmatic and asthmatic airway smooth muscle.
2018-10-22 | GSE119578 | GEO
Project description:The goal of the was to evaluate the mRNA expression profile of asthmatic and non-asthmatic airway smooth muscle using Next Generation Sequencing (RNA seq).
2018-10-22 | GSE119579 | GEO
Project description:Persistent severe asthma is associated with hyper-contractile airways and structural changes in the airway wall, including an increased airway smooth muscle (ASM) mass. This study used gene expression profiles from asthmatic and healthy airway smooth muscle cells grown in culture to identify novel receptors and pathways that potentially contributed to asthma pathogenesis. We used microarrays to compare the gene expression between asthmatic and healthy airway smooth muscle cells to understand the underlying pathway contributing the differences in cellular phenotypes
2015-01-31 | GSE63383 | GEO
Project description:We report the application of RNA sequencing technology for high-throughput profiling of gene expression responses to human rhinovirus infection at 24 hours in air-liquid interface human airway epithelial cell cultures derived from 6 asthmatic and 6 non-asthmatic donors. RNA-seq analysis identified sets of genes associated with asthma specific viral responses. These genes are related to inflammatory pathways, epithelial remodeling and cilium assembly and function, including those described previously (e.g. CCL5, CXCL10 and CX3CL1), and novel ones that were identified for the first time in this study (e.g. CCRL1, CDHR3). We concluded that air liquid interface cultured human airway epithelial cells challenged with live HRV are a useful in vitro model for the study of rhinovirus induced asthma exacerbation, given that our findings are consistent with clinical data sets. Furthermore, our data suggest that abnormal airway epithelial structure and inflammatory signaling are important contributors to viral induced asthma exacerbation. Differentiated air-liquid interface cultured human airway epithelial cell mRNA profiles from 6 asthmatic and 6 non-asthmatic donors after 24 hour treatment with either HRV or vehicle control were generated by deep sequencing, using Illumina HiSeq 2000.
2015-03-01 | E-GEOD-61141 | biostudies-arrayexpress
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:AGING REGULATES VIRUS-TRIGGERED ASTHMATIC AIRWAY PATHOLOGY
| PRJNA768414 | ENA
Project description:T cells promote inflammation in asthmatic patients and both Th2 and Th17 CD4 T cells have been implicated in severe forms of the disease. The metabolic phenotypes and dependencies of these cells, however, remain poorly understood in the regulation of airway inflammation. Here we show the bronchoalveolar lavage fluid of asthmatic patients had markers of elevated glucose and glutamine metabolism. Further, peripheral blood T cells of asthmatics had broadly elevated expression of metabolic proteins when analyzed by mass cytometry compared to healthy controls. Therefore, we hypothesized that glucose and glutamine metabolism were important in allergic airway inflammation. We tested this hypothesis in two murine models of airway inflammation. T cells from lungs of mice sensitized with Alternaria alternata extract displayed genetic signatures for elevated glucose and oxidative metabolism by single cell RNAseq. This result was most pronounced when protein levels were measured in IL17 producing cells and was recapitulated when airway inflammation was induced with House Dust Mite plus lipopolysaccharide (HDM+LPS), a model which led to abundant IL4 and IL17 producing T cells. Importantly, inhibitors of the glucose transporter 1 (Glut1) or glutaminase (GLS) in vivo attenuated HDM+LPS eosinophilia, T cell cytokine production, and airway hyperresponsiveness as well as augmented the immunosuppressive properties of dexamethasone. These data show that T cells induce markers to support metabolism in vivo in airway inflammation and that this correlates with inflammatory cytokine production. Targeting metabolic pathways may provide a new direction to protect from disease and enhance the effectiveness of steroid therapy.
2021-01-13 | GSE163572 | GEO
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.
2015-03-01 | GSE57772 | GEO