Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA93179 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Sputum cell gene expression following allergen challenge
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Project description:Fungal allergen extracts-induced gene expression in airway epithelial cells (NCI-H292)
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Project description:This protocol outlines a single-site mechanistic study aiming to investigate long RNAs differentially expressed in the airway epithelium of asthma patients both at baseline and in response to segmental airway allergen challenges. Over approximately 14 days, the study spanned three visits: Visit 1: Comprehensive characterization of participants, encompassing lung function testing, methacholine challenge testing, and allergen skin prick testing. Visit 2: Participants underwent bronchoscopy wherein three procedures were performed a. Epithelial brushings were performed in a segmental airway (baseline sample) b. Diluent (inactive control) was instilled into another segmental airway c. A small dose of allergen was administered into a third segmental airway using standardized cat or dust mite allergen extracts. Visit 3 (24 hours or 7 days post Visit 2): Another bronchoscopy was carried out to collect epithelial brushings in the diluent challenged and allergen challenged segments The collected epithelial brush samples underwent analysis for mRNA expression in the epithelial brushings. The study successfully incorporated a total of 23 subjects, which included 18 asthmatics (with stable or well-controlled conditions), 2 allergic non-asthmatics, and 3 non-allergic non-asthmatics.
2024-03-08 | GSE250241 | GEO
Project description:Using a human model of asthma exacerbation, we compared the airway mucosa in allergic asthmatics and allergic non-asthmatic controls using single-cell RNA-sequencing frameworks. In response to allergen challenge, the airway epithelium in asthmatics was highly dynamic and upregulated genes involved in matrix degradation, mucus metaplasia, and glycolysis while failing to induce injury-repair and antioxidant pathways observed in controls. Asthmatics also had a unique mucosal immune profile, characterized by IL9-expressing pathogenic TH2 cells and enrichment of DC2 (CD1C) and CCR2-expressing monocyte-derived cells (MC) after allergen, with upregulation of genes that promote pathologic airway remodeling. In contrast, controls were enriched for macrophage-like MC that upregulated tissue repair programs after allergen challenge, suggesting these populations may protect against asthmatic airway remodeling. These findings reveal a novel TH2-mononuclear phagocyte-epithelial interactome unique to asthmatics, suggesting that pathogenic effector circuits and the absence of pro-resolution programs drive structural airway disease in response to type 2 inflammation.
2023-02-24 | GSE193816 | GEO
Project description:Allergen induced gene expression of airway epithelial cells shows a possible role for TNF-α
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Project description:Effects of cigarette smoke on the human airway epithelial cell transcriptome
| PRJNA88045 | ENA
Project description:Allergen exposure induces the airway epithelium to produce chemoattractants, proallergic interleukins, matrix-modifying proteins, and proteins that influence the growth and activation state of airway structural cells. These proteins, in turn, contribute to the influx of inflammatory cells and changes in structure that characterize the asthmatic airway. To use the response of the airway epithelium to allergen to identify genes not previously associated with allergic responses, we compared gene expression in cytokeratin-positive cells before and after segmental allergen challenge. After challenge with concentrations of allergen in the clinically relevant range, 755 (6%) of the detectable sequences had geometric mean fold-changes in expression, with 95% confidence intervals that excluded unity. Using a prospectively defined conservative filtering algorithm, we identified 141 sequences as upregulated and eight as downregulated, with confirmation by conventional polymerase chain reaction in all 10 sequences studied. Using this approach, we identified asthma-associated sequences including interleukin (IL-)-3, IL-4, and IL-5 receptor subunits, the p65 component of nuclear factor-kappaB, and lipocortin. The genomic response of the human airway to concentrations of allergen in the clinically relevant range involves a greater number of genes than previously recognized, including many not previously associated with asthma that are differentially expressed after airway allergen exposure. Keywords: Before and after allergen challenge
2005-08-01 | GSE3004 | GEO
Project description:Allergen exposure induces the airway epithelium to produce chemoattractants, proallergic interleukins, matrix-modifying proteins, and proteins that influence the growth and activation state of airway structural cells. These proteins, in turn, contribute to the influx of inflammatory cells and changes in structure that characterize the asthmatic airway. To use the response of the airway epithelium to allergen to identify genes not previously associated with allergic responses, we compared gene expression in cytokeratin-positive cells before and after segmental allergen challenge. After challenge with concentrations of allergen in the clinically relevant range, 755 (6%) of the detectable sequences had geometric mean fold-changes in expression, with 95% confidence intervals that excluded unity. Using a prospectively defined conservative filtering algorithm, we identified 141 sequences as upregulated and eight as downregulated, with confirmation by conventional polymerase chain reaction in all 10 sequences studied. Using this approach, we identified asthma-associated sequences including interleukin (IL-)-3, IL-4, and IL-5 receptor subunits, the p65 component of nuclear factor-{kappa}B, and lipocortin. The genomic response of the human airway to concentrations of allergen in the clinically relevant range involves a greater number of genes than previously recognized, including many not previously associated with asthma that are differentially expressed after airway allergen exposure. <br><br> NOTE: There is no subject #4 in this series (subject 4 was excluded based on clinical criteria). [For references see publication: Lilly et al., Am J Respir Crit Care Med. 2005 Mar 15;171(6):579-86]
2007-11-21 | E-GEOD-3004 | biostudies-arrayexpress
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression.
2011-02-19 | GSE20463 | GEO
Project description:Expression microarrays identified 119 genes that were significantly differentially expressed in the epithelium of WT and M-NM-26 KO mice after saline or chronic allergen challenge. PAM clustering revealed two interesting clusters (6 and 8) that we had not identified in previous comparisons by whole lung microarrays. Cluster 6 genes were low at baseline in both WT and M-NM-26 KO mice and were increased in WT but not in M-NM-26 KO mice after chronic allergen challenge such as Mcpt1. Cluster 8 genes were increased at baseline in M-NM-26 KO mice, and included 6 mast cell related genes (cma1, mcpt4, cpa3, mcpt6, tpsab1, il1rl1). The most informative differentially expressed genes identified in microarrays of the epithelial microenvironment were not epithelial genes, but mast cell genes. Control and beta6 ko mice (wt-S (4), wt-OVA (4), ko-S (4), ko-OVA (4)) were sensitized and challenged with OVA or saline, airway epithelium were brush-harvested.
2012-12-31 | E-GEOD-28168 | biostudies-arrayexpress