Project description:RNA from cultured human bronchial epithelial cells treated for 8 hours or for 24 hours with medium alone, interferon gamma, dexamethasone or both interferon gamma and dexamethasone. Keywords = interferon gamma Keywords = dexamethasone Keywords = human bronchial epithelial cells Keywords: dose response
Project description:mRNA expression was assayed from bronchial epithelial cells collected via bronchoscopy from healthy current and never smoker volunteers in order to determine relationships between microRNA and mRNA expression in bronchial epithelial cell samples across current and never smokers and within the same individual. Keywords: Global mRNA expression profiling Overall design: Bronchial epithelial cells were collected from current and never smokers via bronchoscopy. High molecular weight RNA ( > 200 nucleotides) was isolated and hybridized to Affymetrix Human Exon 1.0 ST microarrays to obtain mRNA expression from the airway epithelial cells of current and never smokers, which could be correlated to microRNA expression from the same samples.
Project description:The F508del mutation, the most frequent in cystic fibrosis (CF), impairs the maturation of the CFTR chloride channel. The F508del defect can be partially overcome at low temperature (27 °C) or with pharmacological correctors. The rescue elicited by low temperature may involve a direct stabilization of mutant CFTR protein and/or a change in cell transcriptome that creates a more favorable proteostasis environment. To assess the effect of low temperature on gene expression we investigated the transcriptome of bronchial epithelial cells derived from CF with F508del mutation. Cells were kept under control conditions or incubated at 27 °C. Microarray data indicate that hypothermia induces a profound and global change in gene expression that may be in part responsible for rescue of F508del-CFTR. Bronchial epithelial cells from cystic fibrosis patients homozygotes for F508del mutation were isolated. Cells differentiated as epithelial monolayers on porous membranes (Snapwell inserts) were incubated for 24 hours at 27 °C or kept under control conditions. Rescue of mutant CFTR channel by low temperature was checked by measuring transepithelial chloride currents with the Ussing chamber technique. Total RNA was extracted from treated and control cells to assess changes in gene expression with microarrays.
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 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.
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. Overall design: Examination of open chromatin regions by DNase-seq and gene expression by RNA-seq in HBE (primary human bronchial epithelial cells from healthy donors), CFHBE (primary human bronchial epithelial cells from donors with Cystic Fibrosis), HTE (primary human tracheal epithelial cells from healthy donors) and NHBE (Lonza CC-2451 primary human bronchial and tracheal epithelial cells from healthy donors)
Project description:MicroRNA expression was assayed from bronchial epithelial cells collected via bronchoscopy from healthy current and never smoker volunteers in order to determine the effect of cigarette smoke exposure on airway epithelial microRNA expression Keywords: Global microRNA expression profiling Bronchial epithelial cells were collected from current and never smokers via bronchoscopy. Low molecular weight RNA ( < 200 nucleotides) was isolated and hybridized to Invitrogen NCode microRNA microarrays to determine which microRNAs detected in bronchial epithelial cells were differentially expressed in the airways of smokers.
Project description:mRNA expression was assayed from bronchial epithelial cells collected via bronchoscopy and nasal epithelial cells collected by brushing the inferior turbinate from healthy current and never smoker volunteers in order to determine the relationship between smoking-related gene expression changes in bronchial and nasal epithelium within the same individual. Bronchial epithelial cells were collected from current and never smokers via bronchoscopy, and nasal epithelial cells were collected by brushing the inferior turbinate during the same clinic visit. 1ug of RNA was isolated and hybridized to Affymetrix Human Exon 1.0 ST microarrays to obtain mRNA expression. The genome build upon which transcript assignments are based is hg18 (HuEx-1_0-st-v2.na27.hg18.transcript.csv).
Project description:Goblet cell hyperplasia (GCH) is a feature of respiratory diseases characterized by mucus hypersecretion. GCH is driven by Th2 cytokines such as IL-4. To investigate the gene expression changes associated with GCH, we treated human bronchial epithelial cells with IL-4. By microarray analysis and functional studies, we found that IL-4 promotes a profound change that results in enhanced bicarbonate secretion. This change may be required to support mucus release. Overall design: Human bronchial epithelial cells were differentiated as epithelial monolayers on porous membranes (Snapwell inserts). After treatment with IL-4, gene expression changes were determined with microarrays. In parallel, ion transport, mucus release, intracellular pH, and apical fluid composition were measured.