Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA191531 | ENA |
REPOSITORIES: ENA
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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:Pandemic H1N1 influenza A (H1N1pdm) elicits stronger pulmonary inflammation than previously circulating seasonal H1N1 influenza A (sH1N1), yet mechanisms of inflammatory activation in respiratory epithelial cells during H1N1pdm infection are unclear. We investigated host responses to H1N1pdm / sH1N1 infection and virus entry mechanisms in primary human bronchial epithelial cells in vitro. H1N1pdm infection rapidly initiated a robust inflammatory gene signature (3 h post-infection) not elicited by sH1N1 infection. Protein secretion inhibition had no effect on gene induction. Infection with membrane fusion deficient H1N1pdm failed to induce robust inflammatory gene expression which was rescued with restoration of fusion ability, suggesting H1N1pdm directly triggered the inflammatory signature downstream of membrane fusion. Investigation of intra-virion components revealed H1N1pdm viral RNA (vRNA) triggered a stronger inflammatory phenotype than sH1N1 vRNA. Thus, our study is first to report H1N1pdm induces greater inflammatory gene expression than sH1N1 in vitro due to direct virus-epithelial cell interaction. Total RNA obtained from Normal Human Bronchial Epithelial Cells (NHBEC) at 3 hours or 24 hours post-infection with either 0.9 MOI A/Mexico/4108/2009 (H1N1) or 0.9 MOI A/Brisbane/59/2007 (H1N1). Total RNA was also collected at 0 hours from uninfected NHBEC for each infection. Changes in gene expression relative to uninfected cells were then investigated.
2016-07-04 | E-GEOD-48575 | biostudies-arrayexpress
Project description:Cigarette smoke (CS) is a major risk factor in the development of chronic inflammatory lung diseases such as chronic obstructive pulmonary disease. To evaluate the biological impact of CS on lung tissue, three-dimensional (3D) organotypic bronchial tissue cultures can be used to replicate in vivo conditions. We developed an original 3D human bronchial epithelial co-culture model to assess the biological impact of repeated CS exposure on cell differentiation and on the inflammatory response. We found that CS can disrupt homeostatic capacity in a dose-dependent manner, and that the activation of the EGFR pathway, which is involved in the early-stage pathogenesis of airway diseases, was predicted from transcriptomic data. We believe that our model of bronchial tissues, used for repeated CS exposure, can provide valuable information on tissue-specific alterations in biological systems.
2018-09-30 | E-MTAB-6175 | biostudies-arrayexpress
Project description:This present study is the first to investigate the global changes in host gene expression during the interaction of human bronchial epithelial cells and live Alternaria spores. Human bronchial epithelial cells (BEAS2-B) were exposed to spores or media alone for 24 hours. RNA was collected from three biological replicates/treatment and used to assess changes in gene expression patterns using Affymetrix Human Genome U133 Plus 2.0 Arrays. Interestingly, many cytokine/chemokine immune response genes were upregulated. Genes involved in cell death, retinoic acid signaling, TLR3, and interferon response pathways were also significantly upregulated.
2011-12-01 | GSE32893 | GEO
Project description:This present study is the first to investigate the global changes in host gene expression during the interaction of human bronchial epithelial cells and live Alternaria spores. Human bronchial epithelial cells (BEAS2-B) were exposed to spores or media alone for 24 hours. RNA was collected from three biological replicates/treatment and used to assess changes in gene expression patterns using Affymetrix Human Genome U133 Plus 2.0 Arrays. Interestingly, many cytokine/chemokine immune response genes were upregulated. Genes involved in cell death, retinoic acid signaling, TLR3, and interferon response pathways were also significantly upregulated. Three biological replicates for control (untreated cells) and treatment (5 x 10^5 A. alternata spores)
2011-12-01 | E-GEOD-32893 | biostudies-arrayexpress
Project description:Nitric oxide induces p53-mediated cell death in human nasal epithelial cells
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Project description:Ambient O2 pressure induces NF-kB1/RelA related inflammatory response in human lung epithelial cells in vitro
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Project description:Ambient O2 pressure induces NF-kB1/RelA related inflammatory response in human lung epithelial cells in vitro
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Project description:Expression data from human bronchial epithelial cells
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