Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-6802
PROVIDER: PRJNA99201 | ENA |
REPOSITORIES: ENA
Similar Datasets
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. Keywords: expression profiling, response to pathogens
2007-02-27 | GSE6802 | GEO
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
Project description:The mucus secreted by airway epithelial cells plays a key role in the protection against and clearance of particles and pathogens. In this project, a 3D model of the bronchial epithelium was established using Calu-3 cells grown on porous inserts at the air-liquid interface. The secreted proteins were characterized in long-term cultures and compared to the apical secretome of primary normal human bronchial epithelial (NHBE) cells. The apical secretome was collected and characterized in the Calu-3 model at day 4, day 11, and day 18 after air-liquid interface and in the NHBE model at day 4, day 12, and day 18 after air-liquid interface. "This project received funding from the European Union’s Horizon 2020 research and innovation program under grant agreement no 760928 (BIORIMA)."
2021-03-26 | PXD024242 | Pride
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
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 NFκB and TNF-α, 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.
2013-05-27 | GSE44747 | GEO
Project description:We performed RNA sequencing of gene expression of differentiated primary human bronchial epithelial cells derived from control and asthmatic patients, stimulated with IL-13. The Type 2 Asthma mediator IL-13 was described to induce airway hyperresponsiveness, goblet cell metaplasia, mucus hypersecretion and airway remoddeling including impairment of epithelial barrier integrity. We investigated differential expression of SARS-CoV-2 related host gene expression as well as genes involved in N-linked glycosylation upon IL-13 in bronchial epithelial cells. Top IL-13 affected pathways included ion- and transmembrane transport, lipid metabolic processed and protein glycosylation.
2023-01-30 | GSE206510 | GEO
Project description:The epithelial layer lining the airways has a central role in maintaining lung health, particularly serving as a barrier to prevent infection and delivery of harmful particles, which are cleared from the lung on the mucociliary escalator driven by the epithelium. Robust methods to culture primary airway epithelial cells were developed several decades ago and these cells provide the model of choice to investigate many diseases of the human lung. However, to date the molecular signature of cells from different regions of the airway epithelium has not been well characterized. Here we examine primary cells derived from human tracheal and bronchial tissues and perform genome-wide analysis of their active regulatory elements and gene expression profiles. We also compare cells from healthy and diseased (cystic fibrosis) donor lung tissue. Our data reveal an airway cell signature that is divergent from other epithelial cell types and from immortalized or transformed airway epithelial cell lines. The differences between tracheal and bronchial cells are clearly evident as are common regulatory features between the cell types of two different origins. Only minor variation is seen between cells from healthy or CF bronchial cells. These data are a valuable resource for functional genomics analysis of airway epithelial tissues in human health and disease.
2018-02-28 | GSE101993 | GEO
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
Project description:We investigated proteins identified by shotgun proteomics in cytologically normal airway epithelial cells from individuals at different levels of risk for lung cancer. We identified 2869 proteins in bronchial brushings from individuals at low, moderate or high risk for lung cancer. Pathway analysis revealed enrichment of carbohydrate metabolic pathways in high risk individuals. Differential expression of selected proteins was validated by parallel reaction monitoring mass spectrometry in separate individual bronchial brushings. Augmentation of glucose consumption and lactate production measured in human bronchial epithelial cell BEAS2B treated with cigarette smoke condensate and increased synthetic ability and reductive carboxylation revealed by metabolic flux analysis indicated profound metabolic reprogramming.
| MSV000079331 | MassIVE
Project description:Normal human bronchial epithelial (NHBE) cells cultured in an air-liquid interface (ALI) system form a polarized, pseudostratified epithelium composed of basal, ciliated and goblet cells that closely resemble the in vivo airway epithelium structure. ALI cultures of NHBE cells provide a unique in vitro system to investigate airway epithelial biology, including developmental, structural and physiologic aspects. In this study, we wanted to investigate mRNA expression patterns during airway epithelium differentiation. By using microarrays, we studied the changes in expression of mRNAs in normal human bronchial epithelial cells as they differentiate from an undifferentiated monolayer to a differentiated pseudostratified epithelium after 28 days of air-liquid interface (ALI) culture, when epithelial cells differentially express basal, ciliated and goblet cell markers. Normal human bronchial epithelial cells were cultured in an air-liquid interface (ALI) system and harvested at three different time-points: subconfluent, confluent and day 28 of ALI. Samples were processed for total RNA extraction and hybridization on Affymetrix microarrays. All the experiments were performed by triplicate.
2012-10-01 | E-GEOD-39059 | biostudies-arrayexpress