Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA87945 | ENA |
REPOSITORIES: ENA
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Project description:This series contains 5 groups of U133A arrays with targets from Calu-3 cell line post-infection with P aeruginosa strains. Calu-3 human lung epithelial cells were seeded onto 6-well plates and grown to about 80% confluency. Epithelial monolayers were infected with 108 CFUs per ml of each bacterial strain for 60 min and then washed extensively with phosphate-buffered saline. The cultures were subsequently incubated in fresh RPMI 1640 medium supplemented with 10% fetal bovine serum and 100 µg/ml gentamicin. After 6 h, total RNA from the cells was prepared with RNAzol and further purified with RNEasy for microarray hybridization. All arrays processed and globally scaled to 500 using MAS 5. CONTROL (4 arrays) - no infection FRD1 (4 arrays) FRD1234 (3 arrays) FRD440 (4 arrays) FRD875 (4 arrays) Keywords = Cystic Fibrosis Keywords = Pseudomonas aeruginosa Keywords = CF Keywords = flagellin Keywords = alginate Keywords = lung Keywords: repeat sample
2004-10-08 | GSE923 | GEO
Project description:A complex network of transcription factors regulates genes involved in establishing and maintaining key biological properties of the human airway epithelium. Here we characterize the role of Krüppel-Like Factor 5 (KLF5), in controlling essential pathways of epithelial cell identity and function in the human lung. RNA-seq following siRNA-mediated depletion of KLF5 in the Calu-3 lung epithelial cell line identified significant enrichment of genes encoding chemokines and cytokines involved in the proinflammatory response, and also components of the junctional complexes mediating cell adhesion. To determine direct gene targets of KLF5, we defined the cistrome of KLF5 using ChIP-seq in both Calu-3 and 16HBE14o- lung epithelial cells lines. Occupancy site concordance analysis revealed that KLF5 co-localized with the active histone modification H3K27ac and also with binding sites for CCAAT Enhancer Binding Protein Beta (C/EBPβ). Depletion of KLF5 increased both the expression and secretion of important chemokines, a response that was enhanced following exposure to Pseudomonas aeruginosa lipopolysaccharide. Wound scratch assays in Calu-3 cells exhibited faster rates of repair after KLF5 depletion than did negative controls. Similarly, CRISPR-mediated KLF5-null 16HBE14o- cells also showed enhanced wound closure. These data reveal a pivotal role for KLF5 in coordinating epithelial functions relevant to human lung disease.
2021-10-07 | GSE164852 | GEO
Project description:A complex network of transcription factors regulates genes involved in establishing and maintaining key biological properties of the human airway epithelium. Here we characterize the role of Krüppel-Like Factor 5 (KLF5), in controlling essential pathways of epithelial cell identity and function in the human lung. RNA-seq following siRNA-mediated depletion of KLF5 in the Calu-3 lung epithelial cell line identified significant enrichment of genes encoding chemokines and cytokines involved in the proinflammatory response, and also components of the junctional complexes mediating cell adhesion. To determine direct gene targets of KLF5, we defined the cistrome of KLF5 using ChIP-seq in both Calu-3 and 16HBE14o- lung epithelial cells lines. Occupancy site concordance analysis revealed that KLF5 co-localized with the active histone modification H3K27ac and also with binding sites for CCAAT Enhancer Binding Protein Beta (C/EBPβ). Depletion of KLF5 increased both the expression and secretion of important chemokines, a response that was enhanced following exposure to Pseudomonas aeruginosa lipopolysaccharide. Wound scratch assays in Calu-3 cells exhibited faster rates of repair after KLF5 depletion than did negative controls. Similarly, CRISPR-mediated KLF5-null 16HBE14o- cells also showed enhanced wound closure. These data reveal a pivotal role for KLF5 in coordinating epithelial functions relevant to human lung disease.
2021-10-07 | GSE164851 | GEO
Project description:This series contains 5 groups of U133A arrays with targets from Calu-3 cell line post-infection with P aeruginosa strains. Calu-3 human lung epithelial cells were seeded onto 6-well plates and grown to about 80% confluency. Epithelial monolayers were infected with 108 CFUs per ml of each bacterial strain for 60 min and then washed extensively with phosphate-buffered saline. The cultures were subsequently incubated in fresh RPMI 1640 medium supplemented with 10% fetal bovine serum and 100 µg/ml gentamicin. After 6 h, total RNA from the cells was prepared with RNAzol and further purified with RNEasy for microarray hybridization. All arrays processed and globally scaled to 500 using MAS 5. CONTROL (4 arrays) - no infection; FRD1 (4 arrays); FRD1234 (3 arrays); FRD440 (4 arrays); FRD875 (4 arrays)
2007-09-28 | E-GEOD-923 | biostudies-arrayexpress
Project description:We previously showed that pre-exposure of the cornea to TLR5 ligand flagellin induces profound mucosal innate protection against pathogenic microbes by reprogramming gene expression. To date, there was no genome-wide cDNA array to detect full scale of flagellin mediated reprogramming of gene expression in mucosal surface epithelial cells. Taking advantage of readily accessible, easily procurable epithelial cell population, this study is the first report to use genome-wide cDNA microarray approach to document genes associated with flagellin-induced protection against Pseudomonas aeruginosa infection in corneal epithelial cells (CECs). Total RNA obtained from isolated mouse corneal epithelial cells of the control (cells scrapped off from the corneas without infection), Pseudomonas aeruginosa infected (6 h post infection) and flagellin pretreated (24 h), followed by Pseudomonas aeruginosa infection (6 h).
2013-01-01 | E-GEOD-41147 | biostudies-arrayexpress
Project description:Purpose: To determine effects of arsenic on gene expression in polarized primary human bronchial epithelial (HBE) cells and impact on transcriptional response to Pseudomonas aeruginosa infection Methods: mRNA profiles of HBE cells from 6 donors exposed to 0, 5, 10 or 50 ug/L total arsenic +/- Pseudomonas aeruginosa (48 samples) were generated using Illumina sequencing, aligned in CLC Genomics workbench and analyzed for DE in EdgeR Findings: 20-30 million reads were mapped per sample and transcripts were identifed that were significantly differentially expressed in response to arsenic and Pseudomonas aeruginosa
2017-06-26 | GSE97036 | GEO
Project description:Cystic Fibrosis (CF) is the most common life limiting genetic disorder, characterized by chronic respiratory failure secondary to inflammation and chronic bacterial lung infection. Pseudomonas aeruginosa lung infection is associated with more severe lung disease and rapid progression of respiratory failure when compared to Staphylococcus aureus infection. We hypothesized that a specific signature of epigenetic factors targeting specific gene transcripts contributes to the increased morbidity seen in CF patients with chronic Pseudomonas infection. We collected exhaled breath condensate (EBC) from 27 subjects and evaluated miRNA signatures in these samples using commercial PCR array. We identified predicted mRNA targets and associated signaling pathways using Ingenuity Pathway Analysis. We found 11 differentially expressed miRNAs in EBC of patients infected with Pseudomonas aeruginosa compared to EBC from CF patients who were not chronically infected with Pseudomonas aeruginosa.
2019-04-22 | GSE130159 | GEO
Project description:RNA-seq was performed to study the transcriptomic changes in human lung tissue post infection with either Influenza A virus (IAV), or Pseudomonas aeruginosa (PA) or Mycobacterium bovis (BCG)
2021-12-30 | GSE192528 | GEO
Project description:small non-coding RNA-seq was performed to study the transcriptomic changes in human lung tissue post infection with either Influenza A virus (IAV), or Pseudomonas aeruginosa (PA) or Mycobacterium bovis (BCG)
2022-01-04 | GSE192864 | GEO
Project description:The purpose of the study is to compare the transcriptomic profile of the airway epithelial cell line Calu-3 in reponse to Pseudomonas aeruginosa virulence factor flagellin. CF is caused by mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene. CFTR gene in Calu-3 cells was knockdown by CRISPR-Cas9 (TS) and a control cell line (CTL) was aslo generated using a non-targeting guide RNA. CTL and CFTR KD Calu3-cells were grown on Transwell filters, polarized at the air-liquid interface and exposed to flagellin for 6 hours. We considered 2 non-stimulated (ND) conditions: CTL-NS and TS-NS, and 2 conditions stimulated with flagellin (Flag): CTL-Flag and TS-Flag.
2020-08-24 | GSE133495 | GEO