Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression analysis of bronchial epithelial cells stimulated by different airway pathogens.

ABSTRACT: Bronchial epithelial cells represent the first line of defense against invading airborne pathogens. They are important contributors to innate mucosal immunity and provide a variety of anti-microbial effectors. To investigate the role of epithelial cells upon infection of airway pathogens, we stimulated BEAS-2B cells for 4 h with UV-inactivated bronchial pathogens including Staphylococcus aureus, Pseudomonas aeruginosa and Respiratory Syncitial Virus (RSV) that among other receptors can strongly activate TLR2, TLR4 and TLR3, respectively. Keywords: expression profiling, response to pathogens

ORGANISM(S): Homo sapiens

PROVIDER: GSE6802 | GEO | 2007/02/27

SECONDARY ACCESSION(S): PRJNA99201

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcription profiling of human bronchial airway epithelial cells infected with P. aeruginosa, S.aureus or respiratory syncytial virus vs uninfected controls to investigate the role of epithelial cells upon infection of airway pathogens

Project description:Bronchial epithelial cells represent the first line of defense against invading airborne pathogens. They are important contributors to innate mucosal immunity and provide a variety of anti-microbial effectors. To investigate the role of epithelial cells upon infection of airway pathogens, we stimulated BEAS-2B cells for 4 h with UV-inactivated bronchial pathogens including Staphylococcus aureus, Pseudomonas aeruginosa and Respiratory Syncitial Virus (RSV) that among other receptors can strongly activate TLR2, TLR4 and TLR3, respectively. Experiment Overall Design: All conditions were done in triplicates except for Staphylococcus aureus, were two replicates were done. As a control, unstimulated BEAS-2B were used. Altogether 11 arrays were hybridized.

2007-11-11 | E-GEOD-6802 | biostudies-arrayexpress

RSV gene expression

Project description:Human bronchial epithelial cells (BEAS-2B cells) were treated with RSV at 1.0 MOI for 4 and 24 hours or control (vehicle-treated for 4 hours). Global gene expression was measured by Affy Hu133 plus 2.0 microarray chips. Keywords: Inflammation, microtubules, RSV, time course

2006-05-01 | GSE3397 | GEO

Transcription profiling of human bronchial epithelial cells treated with respiratory syncytial virus (RSV) for 4 and 24 hours

Project description:Human bronchial epithelial cells (BEAS-2B cells) were treated with RSV at 1.0 MOI for 4 and 24 hours or control (vehicle-treated for 4 hours). Global gene expression was measured by Affy Hu133 plus 2.0 microarray chips. Experiment Overall Design: 4 controls (vehicle-treated for 4 hours) Experiment Overall Design: 4 RSV-treated for 4 hours Experiment Overall Design: 4 RSV-treated for 24 hours

2007-10-02 | E-GEOD-3397 | biostudies-arrayexpress

PKC Activation Induces Inflammatory Response and Cell Death in Human Bronchial Epithelial Cells

Project description:A variety of airborne pathogens can induce inflammatory responses in airway epithelial cells, which is a crucial component of host defence. However, excessive inflammatory responses and chronic inflammation also contribute to different diseases in the respiratory system. We hypothesized that the activation of protein kinase C (PKC) is one of the essential mechanisms of inflammatory responses in airway epithelial cells. In the present study, we stimulated human bronchial lung epithelial (BEAS-2B) cells with phorbol ester Phorbol 12, 13-dibutyrate (PDBu), and examined gene expression profile with microarray analysis. Bioinformatics suggested that PKC activation induced dramatic changes in gene expression related to multiple cellular functions. The top two functional networks of genes were centered on NFM-NM-:B and TNF-M-NM-1, which are two commonly known pathways for cell death and inflammation. Subsequent tests confirmed the decrease in cell viability and increase in the production of various cytokines. Interestingly, each of the increased cytokines was differentially regulated at mRNA and/or protein levels by different sub-class of PKC isozymes. We conclude that many pathogen-induced cell death and cytokine production in airway epithelial cells may be mediated through PKC related signaling pathways. These findings suggest that PKCs can be new targets for treatments of lung diseases. Three groups of BEAS-2B cells were prepared: control, 0.5 hour of PDBu stimulation, and 4 hours of PDBu stimulation. Each group consisted of three biological replicates.

2013-05-27 | E-GEOD-44747 | biostudies-arrayexpress

Homo sapiens

Project description:Airborne particulate matter affects gene expression in BEAS-2B bronchial epithelial cells.

| PRJNA150475 | ENA

MicroRNA levels in non-transformed and transformed lung cells

Project description:MicroRNA levels in non-transformed BEAS-2B bronchial epithelial cells, two lines of mycoplasma transformed BEAS-2B cells, and A549 lung adenocarcinoma cells were measured. Microarray analyses of 1145 microRNAs in A549 lung adenocarcinoma cells and two other transformed lung cell types relative to BEAS-2B bronchial epithelial cells were performed. 106 miRNAs were down-regulated and 69 miRNAs were up-regulated in all three transformed lines

2014-03-11 | GSE55748 | GEO

TGF-beta treated airway epithelium

Project description:Despite being exposed to respiratory syncytial virus (RSV) infection multiple times in our lives, infants, older-adults, and immunocompromised patients are vulnerable to RSV-associated severe diseases, such as bronchiolitis and pneumonia. Respiratory viral infections are known to promote pulmonary fibrosis formation, which are often associated with a cellular remodeling process epithelial-mesenchymal transition (EMT). However, there is no information on whether RSV causes EMT in bronchial epithelial cells. Our results suggest that RSV-infection does not induce EMT in three different in vitro lung models: epithelial A549 cell line, primary normal human bronchial epithelial cells, and pseudostratified airway epithelium. Interestingly, RSV infection increased cell surface area and perimeter in the infected airway epithelium, which is distinct from the TGF-β1 driven cell elongation. Genome-wide transcriptome analysis also revealed that RSV infection is not involved in cell motility and locomotion. Thus, our results suggest that RSV infection does not induce EMT in the airway epithelium

2023-06-13 | GSE189537 | GEO

Next Generation Sequencing Analysis of miRNA profiling in Epithelial Type and Mesenchymal Type Beas-2b Cells

Project description:We reported the application of next generation sequencing technology for high-throughput profiling of miRNA expression in bronchile epithelial cell line Beas-2b with epithelial or mesenchymal mophology. By comparation the expression aboundence of known miRNAs between epithelial type and mesenchymal type Beas-2b cells, we found both upregulated and downregulated miRNAs in bronchial epithelial cells during EMT. This study provides a basic condition for further investigation of the roles of the regulated miRNAs during EMT in bronchial epithelial cells.

2018-12-26 | GSE117522 | GEO

m6A-mRNA&lncRNA Epitranscriptomic Microarray

Project description:Total RNA samples from human bronchial epithelial BEAS-2B passage-matched control cells and Cr(VI)-transofmred BEAS-2B cells were submitted to ArraySatr for total RNA m6A epitranscriptomic microarray analysis

2022-06-29 | GSE186605 | GEO

Transcription profiling of human bronchial epithelial cells stimulated with the commensal bacterium S. salivarius K12 of the pathogens S. aureus, P. aeruginosa, or S. enteritidis

Project description:Human bronchial epithelial cells (16HBE14O-) were stimulated with the commensal bacterium S. salivarius K12, or the pathogens S. aureus, P. aeruginosa, or S. enteritidis (subtype Typhimurium) for 1 hour.

2008-10-30 | E-FPMI-13 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data