Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA127535 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We compared the gene expression stimulated with fungal extracts from Aspergillus (A.) fumigatus, Alternaria (A.) alternata, or Penicillium (P.) notatum in NCI-H292 (a human bronchial epithelial cell line) to search Allergic bronchopulmonary mycosis (ABPM)-related genes. We identified a mucin-related MUC5AC gene, the expression of which was selectively induced by A. fumigatus. Total RNA from NCI-H292 cells stimulated for 24 h with the A. fumigatus, A. alternata, or P. notatum fungi extracts was extracted and subjected to microarray analysis. Each experiments were perfomed once for each stimulus.
2011-07-07 | E-GEOD-22323 | biostudies-arrayexpress
Project description:We compared the gene expression stimulated with fungal extracts from Aspergillus (A.) fumigatus, Alternaria (A.) alternata, or Penicillium (P.) notatum in NCI-H292 (a human bronchial epithelial cell line) to search Allergic bronchopulmonary mycosis (ABPM)-related genes. We identified a mucin-related MUC5AC gene, the expression of which was selectively induced by A. fumigatus.
2011-07-07 | GSE22323 | GEO
Project description:Response to allergen was studied in bronchial epithelial cell line H292. Cells were cultured and subsequently exposed to House dust mite or vessel (saline) Microarray data was analysed using bioinformatics and biostastics. We find a strong response to allergen in epithelial cells Keywords: cellular response to allergen
2007-10-01 | GSE9151 | GEO
Project description:To investigate the gene expression of lung epithelial cells effected by Trichomonas tenax, we chose NCI-H292 lung epithelial cells and cocultured with Trichomonas tenax.
2024-03-24 | GSE228216 | GEO
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:Effects of allergen challenge on airway epithelial cell gene expression
| PRJNA93179 | ENA
Project description:Allergen induced gene expression of airway epithelial cells shows a possible role for TNF-α
| PRJNA102701 | ENA
Project description:Response to allergen was studied in bronchial epithelial cell line H292. Cells were cultured and subsequently exposed to House dust mite or vessel (saline); Microarray data was analysed using bioinformatics and biostastics. We find a strong response to allergen in epithelial cells Experiment Overall Design: Bronchial epithelial cell line was cultured and stimulated with house dust mite extract or diluent alone. Both conditions were performed in triplicate
2008-06-16 | E-GEOD-9151 | biostudies-arrayexpress
Project description:Background: Environmental allergens can induce epithelial cellular senescence, which contributes to airway inflammation. The aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor responsive to environmental stimuli, may regulate this process. Objectives: We sought to determine whether epithelial AhR controls cellular senescence and to define its underlying mechanisms in allergic airway inflammation. Methods: Club cell-specific p16 conditional knockout mice (p16ΔScgb1a1) were used to assess the role of epithelial senescence and allergic airway inflammation. AhR regulation of senescence was examined using AhR agonist, antagonist, and Club cell-specific AhR-deficient mice (AhRΔScgb1a1) in both in vitro and in vivo models. Bulk RNA-seq was performed to identify AhR-regulated, senescence-associated genes, and immunoprecipitation (IP) along with ChIP-PCR was employed to validate AhR-target gene interactions. Results: Single-cell transcriptomics revealed epithelial senescence as a key feature of allergen-induced asthma. p16ΔScgb1a1 mice exhibited reduced cockroach allergen–induced airway inflammation and decreased Th2/Th17 cytokines in bronchoalveolar lavage fluids (BALFs). AhR signaling was enhanced in airway epithelial cells of allergen-treated asthmatics and regulated senescence, as indicated by SA-β-gal activity and expression of Cdkn2a, Cdkn1a, and γH2AX. The AhR agonist VAF347 suppressed, whereas AhRΔScgb1a1 deficiency exacerbated, airway inflammation. RNA-seq identified senescence as a major AhR-regulated pathway, highlighting c-Myc, TGF-β2, IGFBP3, and SERPINE1 as key targets. AhR binding to the c-Myc promoter was validated, and c-Myc inhibition with EN4 reduced allergen-induced senescence and inflammation. Conclusions: Epithelial AhR suppresses allergen-induced senescence and airway inflammation through direct regulation of c-Myc. These findings establish the AhR–c-Myc axis as a potential therapeutic target in allergic asthma.
2026-03-05 | GSE313889 | GEO