Expression data from mouse lung epithelium after allergen challenge
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ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Taylor Doherty
PROVIDER: E-GEOD-34764 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Allergen exposure induces the airway epithelium to produce chemoattractants, proallergic interleukins, matrix-modifying proteins, and proteins that influence the growth and activation state of airway structural cells. These proteins, in turn, contribute to the influx of inflammatory cells and changes in structure that characterize the asthmatic airway. To use the response of the airway epithelium to allergen to identify genes not previously associated with allergic responses, we compared gene expression in cytokeratin-positive cells before and after segmental allergen challenge. After challenge with concentrations of allergen in the clinically relevant range, 755 (6%) of the detectable sequences had geometric mean fold-changes in expression, with 95% confidence intervals that excluded unity. Using a prospectively defined conservative filtering algorithm, we identified 141 sequences as upregulated and eight as downregulated, with confirmation by conventional polymerase chain reaction in all 10 sequences studied. Using this approach, we identified asthma-associated sequences including interleukin (IL-)-3, IL-4, and IL-5 receptor subunits, the p65 component of nuclear factor-{kappa}B, and lipocortin. The genomic response of the human airway to concentrations of allergen in the clinically relevant range involves a greater number of genes than previously recognized, including many not previously associated with asthma that are differentially expressed after airway allergen exposure. <br><br> NOTE: There is no subject #4 in this series (subject 4 was excluded based on clinical criteria). [For references see publication: Lilly et al., Am J Respir Crit Care Med. 2005 Mar 15;171(6):579-86]
2007-11-21 | E-GEOD-3004 | biostudies-arrayexpress
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).
2011-03-14 | E-GEOD-16008 | biostudies-arrayexpress
Project description:Smoking is the leading cause of lung cancer death, although only a small percentage of smokers develop the disease. Cigarette smoke exposure is known to cause a field of injury in cells throughout the respiratory tract, and while these airway epithelial cells are morphologically normal, they can undergo genetic alterations in response to cigarette smoke exposure. We used microarrays to analyze the gene expression of epithelial cells in the extrathoracic epithelium, specifically nasal and buccal epithelium, to see if these cells underwent similar genetic alterations in response to tobacco exposure as seen in bronchial epithelial cells as has been previously reported. Experiment Overall Design: Buccal and nasal epithelial cell samples were collected from healthy current and never smokers. RNA was isolated from these samples and hybridized to Affymetrix microarrays. Gene expression from never smokers was compared to never smoker gene expression from bronchial epithelium as well as expression data from other tissues to determine commonalities in expression patterns in normal extra- and intra-thoracic samples. In addition, gene expression from smokers and nonsmokers was compared in bronchial, nasal, and buccal epithelium to determine similarities in gene expression in these tissues in response to cigarette smoker exposure.
2008-10-20 | E-GEOD-8987 | biostudies-arrayexpress
Project description:Segmental allergen challenge increases the percentage of eosinophils in bronchoalveolar lavage (BAL) cells. Mepolizumab, an anti-IL-5 therapeutic antibody, decreases the number of eosinophils in bronchoalveolar lavages (BAL). The use of both procedures allows to define genes that are either expressed by eosinophils or dependent on eosinophil presence in the airways. Cells from Bronchoalveolar lavages (BAL) are obtained by bronchoscopy before (V5) and 48 h after a segmental allergen challenge (V6) in atopic and mild astmatics. This procedure was repeated in the same two subjects 2 months later and 1 month after an injection of mepolizumab (V22 is before challenge and V23 after challenge). Cells were immediately lysed and isolated total RNAs were analyzed using the Human Genome 1.0 ST GeneChip arrays (Affymetrix, Santa Clara, CA).
2013-05-01 | E-GEOD-46159 | biostudies-arrayexpress
Project description:A number of studies have shown that cigarette smoking produces a field defect, such that genetic mutations induced by smoking occur throughout the lung and its intra and extra-pulmonary airways. Based on this concept, we have begun this study, which has as its goal the definition of the normal airway transcriptome, an analysis of how that transcriptome is affected by cigarette smoke, and to explore the reversibility of altered gene expression when smoking has been discontinued. We have obtained brushings from intra-pulmonary airways (the right upper lobe carina) and scrapings from the buccal mucosa, from normal smoking and non-smoking volunteers (including 34 Current Smokers, 23 Never Smokers and 18 Former Smokers). RNA was isolated from these samples and gene expression profiles from intra-pulmonary airway epithelial cells were analyzed using Affymetrix U133A human gene expression arrays. All microarray data from the experiments described above have been stored, preprocessed and analyzed in a relational MySQL database that is accessible through our website at http://pulm.bumc.bu.edu/aged
2007-10-04 | E-GEOD-994 | biostudies-arrayexpress
Project description:Rationale: Damage to airway epithelium is followed by deposition of extracellular matrix (ECM) and migration of adjacent epithelial cells. We have shown that epithelial cells from asthmatic children fail to heal a wound in vitro. Objectives: To determine whether dysregulated ECM production by the epithelium plays a role in aberrant repair in asthma. Methods: Airway epithelial cells (AEC) from children with asthma (n=36), healthy atopic (n=23) and healthy non-atopic controls (n=53) were investigated by microarray, gene expression and silencing, transcript regulation analysis and ability to close mechanical wounds. Results: Wound repair of AEC from healthy and atopic children were not significantly different and were both faster than AEC from asthmatics. Microarray analysis revealed differential expression of multiple gene sets associated with repair and remodeling in asthmatic AEC. Fibronectin (FN) was the only ECM component whose expression was significantly lower in asthmatic AEC. Expression differences were verified by qPCR and ELISA, and reduced FN expression persisted in asthmatic cells over passage. Silencing of FN expression in non-asthmatic AEC inhibited wound repair, while addition of FN to asthmatic AEC restored reparative capacity. Asthmatic AEC failed to synthesize FN in response to wounding or cytokine/growth factor stimulation. Exposure to 5â, 2âdeoxyazacytidine had no effect on FN expression and subsequent analysis of the FN promoter did not show evidence of DNA methylation. Conclusions: These data show that the reduced capacity of asthmatic epithelial cells to secrete FN is an important contributor to the dysregulated AEC repair observed in these cells. 16 arrays, 2 experimental groups, asthma atopic, AA, and healthy non-atopic, HN.
2010-04-12 | E-GEOD-18965 | biostudies-arrayexpress
Project description:Changes occur in the lung epithelium after allergen challenge that may give insight into asthma pathogenesis and we sought to identify novelepithelial genes induced by allergen exposure. We used microarrays to identify up-regulated genes induced by allergen challenge in lung epithelium.
2011-12-30 | GSE34764 | GEO
Project description:Bronchial Epithelial Cells were isolated processed as described (Chu et al., 2002 and Zhao et al., 2011). The objective of the study was to identify differentially expressed genes between normal control (NC), mild-moderate asmathic (notSA) and severe asthmatic (SA) patients. For demographics data, contact Dr.Sally Wenzel (wenzelse@upmc.edu) Bronchoscopy with endobronchial epithelial brushing was performed as previously described (Chu et al., 2002; Zhao et al., 2011). The bronchial brushings generally comprised >90% epithelial cells and were placed into Trizol for mRNA analysis. Total RNA extracted using Trizol according to the manufacturer's instructions. Cy3-CTP labeled RNA was prepared according to the standard Agilent protocol from 50ng total RNA. Labeled RNA was hybridized for 17 hr at 65 C on Agilent gene expression array. Arrays were washed according to the manufacturer's protocol. Slides were scanned immediately after washing on the Agilent DNA Microarray Scanner (G2505B) using one color scan setting for 4X44K array slides. Agilent Feature Extraction v10.7.3.1 was used with default parameters. Normalized signal intensity data are presented in the matrix. The data set was normalized by cyclic-LOESS with use of Bioconductor package as described previously (Wu W et. al. 2005)
2014-11-14 | E-GEOD-63142 | biostudies-arrayexpress
Project description:Upregulation of Expression of the Ubiquitin Carboxyl Terminal Hydrolase L1 Gene in Human Airway Epithelium of Cigarette Smokers; The microarray data deposited here is from 44 HuGeneFL GeneChips, from 9 normal non-smokers and 13 phenotypic normal smokers, large airways, 2 samples per individual, one from the right lung and one from the left lung. These samples were previously described in Hackett NR, Heguy A, Harvey BG, O'Connor TP, Luettich K, Flieder DB, Kaplan R, Crystal RG. Variability of antioxidant-related gene expression in the airway epithelium of cigarette smokers. Am J Respir Cell Mol Biol. 2003 29:331-43 and in Heguy A, Harvey BG, O'Connor TP, Hackett NR, Crystal RG. Sampling-dependent up-regulation of gene expression in sequential samples of human airway epithelial cells. Mol Med. 2003 9:200-8. These data are part of a study aimed at understanding how cigarette smoking modifies neuroendocrine cells, in which microarray analysis with TaqMan confirmation was used to assess airway epithelial samples obtained by fiberoptic bronchoscopy from 81 individuals (normal nonsmokers, normal smokers, smokers with early COPD and smokers with established COPD). Of 11 genes considered to be neuroendocrine cell-specific, only ubiquitin C-terminal hydrolase L1(UCHL1), a member of the ubiquitin proteasome pathway, was consistently upregulated in smokers compared to nonsmokers. Up-regulation of UCHL1 at the protein level was observed with immunohistochemistry of bronchial biopsies of smokers compared to nonsmokers. Interestingly, however, while UCHL1 expression was present only in neuroendocrine cells of the airway epithelium in nonsmokers, UCHL1 expression was also expressed in ciliated epithelial cells in smokers, an intriguing observation in light of recent observations that ciliated cells can are capable of transdifferentiating to other airway epithelium. In the context that UCHL1 is involved in the degradation of unwanted, misfolded or damaged proteins within the cell and is overexpressed in >50% of lung cancers, its overexpression in chronic smokers may represent an early event in the complex transformation from normal epithelium to overt malignancy. Experiment Overall Design: comparison of gene expression in airway epithelial cells of the large airways of phenotypic normal smokers vs normal non-smokers
2008-11-07 | E-GEOD-5056 | biostudies-arrayexpress
Project description:Expression data from mouse lung epithelium after allergen challenge
| PRJNA150361 | ENA