Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA127535 | ENA |
REPOSITORIES: ENA
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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: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:Rationale: Aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor, has been considered as an important regulator for immune diseases. We have previously shown that AhR protects against allergic airway inflammation. The underlying mechanism, however, remains undetermined. Objectives: We sought to determine whether AhR specifically in Type II alveolar epithelial cells (AT2) modulates allergic airway inflammation and its underlying mechanisms. Methods: The role of AhR in AT2 cells in airway inflammation was investigated in a mouse model of asthma with AhR conditional knock out mice in AT2 cells (Sftpc-Cre;AhRflox/flox). The effect of AhR on allergen-induced autophagy was examined by both in vivo and in vitro analyses. The involvement of autophagy in airway inflammation was analyzed by using autophagy inhibitor chloroquine. The AhR-regulated gene profiling in AT2 cells was also investigated by RNA-seq analysis. Results: Sftpc-Cre; AhRflox/flox mice showed exacerbation of allergen-induced airway hyperresponsiveness and airway inflammation with elevated Th2 and airway epithelial-derived cytokines in bronchoalveolar lavage fluid (BALF). Notably, an increased allergen-induced autophagy was observed in the lung tissues of Sftpc-Cre; AhRflox/flox mice when compared with wild-type mice. Further analyses suggested a functional axis of AhR-TGF-β1 that is critical in driving allergic airway inflammation through regulating allergen-induced cellular autophagy. Furthermore, inhibition of autophagy suppressed allergic airway inflammation with decreased Th2 and epithelial cell-derived cytokines in BALFs. Additionally, RNA-seq analysis suggests that autophagy is one of the major pathways and CALCOCO2/NDP52 and S1009 are major autophagy-associated genes in AT2 cells that contribute to the AhR-mediated allergic airway inflammation. Conclusion: These results suggest that AhR in AT2 cells functions as a protective mechanism against allergic airway inflammation through controlling cell autophagy.
2022-06-13 | GSE205818 | GEO
Project description:Allergen induced gene expression of airway epithelial cells shows a possible role for TNF-α
| PRJNA102701 | ENA
Project description:Despite the appreciated in vivo role of the redox-active Pseudomonas virulence factor pyocyanin in Pseudomonas airway infections and the recognized importance of airway epithelial cells in combating bacterial pathogens, little is known about pyocyaninM-bM-^@M-^Ys effect on airway epithelial cells. We find that exposure of bronchiolar epithelial cells to pyocyanin results in MUC2/MUC5AC induction and mucin secretion mediated by reactive oxygen species production, activation of the epidermal growth factor receptor pathway and release of inflammatory cytokines (IL-1b, IL-6, TGFa, TNFa). Microarray analysis identified 286 pyocyanin-induced genes in airway epithelial cells, including many of the inflammatory mediators elevated in cystic fibrosis airways (G-CSF, GM-CSF, CXCL1, SAA). We also found several novel pyocyanin-responsive genes of potential importance in the infection process (IL-24, CXCL2, CXCL3, CCL20, SOD2). This comprehensive study uncovers numerous details of pyocyaninM-bM-^@M-^Ys proinflammatory action and establishes airway epithelial cells as key responders following exposure to this microbial toxin. H292 cells were treated with or without 8 uM pyocyanin for 48 hrs in serum-free RPMI medium. RNA was isolated in four independent experiments, collected, processed and subjected to microarray analysis simultaneously (biological repeats).
2011-06-01 | E-GEOD-22430 | biostudies-arrayexpress
Project description:To clarify the role of Caspase-4 in non-small cell lung cancer cells, Caspase-4 overexpressing and knockout cells in NCI-H292 cells were established and each was analyzed by RNAseq.
2023-06-21 | GSE235296 | GEO