Effect of IL-13 on transcriptome of differentiated human airway mucociliary epithelium
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PROVIDER: PRJNA434581 | ENA |
REPOSITORIES: ENA
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Project description:We used microarrays to detail the global programme of gene expression that occurs in response to treatment of IL-13 on fully-differentiated human airway mucociliary epithelium
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2011-06-06 | E-GEOD-22141 | biostudies-arrayexpress
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Project description:The regeneration of the airway mucociliary epithelium involves several sequential events including migration, proliferation, polarization and final differentiation (i.e ciliogenesis). We used microarrays to detail the global programme of gene expression that occurs during regeneration and ciliogenesis of the human airway mucociliary epithelium.
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Project description:The regeneration of the airway mucociliary epithelium involves several sequential events including migration, proliferation, polarization and final differentiation (i.e ciliogenesis). We used microarrays to detail the global programme of gene expression that occurs during regeneration and ciliogenesis of the human airway mucociliary epithelium. The four time points of regeneration of the airway epithelium (ALI-D0 which corresponds to the end of proliferation step; ALI-D7 which corresponds to the polarization step; ALI-D14 which corresponds to the onset of ciliogenesis and ALI-D21 corresponding to the terminal differentiation step) for RNA extraction and hybridization on Affymetrix microarrays.
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Project description:Expression data from airway basal cells and mucociliary-differentiated epithelium of COPD patients and normal subjects
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Project description:Air pollution particulate matter <2.5 microns (PM2.5) is associated with poor respiratory outcomes. Mechanisms underlying PM2.5-induced lung pathobiology are poorly understood, but likely involve cellular and molecular changes to the airway epithelium. We extracted and chemically characterized the organic and water-soluble components of contemporary ambient air pollution PM2.5 samples. We then determined the whole transcriptome responses of human mucociliary airway epithelial cultures (n=12) to a dose series of PM2.5 extracts. We found PM2.5 organic, but not water-soluble, constituents elicited a potent, dose-dependent transcriptomic response from the mucociliary epithelium. Epithelial exposure to a moderate organic extract (OE) dose modified the expression of 424 genes, which included activation of aryl-hydrocarbon receptor (AHR) signaling and an interleukin-1 inflammatory program. We generated an OE response network composed of 8 metagroups, which exhibited high connectivity through the CYP1A1, IL1A, and IL1B genes. This OE exposure also robustly activated a mucus secretory expression program (>100 genes), which included transcriptional drivers of mucus metaplasia (SPDEF, FOXA3). Exposure to a higher OE dose modified the expression of 1,240 genes and further exacerbated expression responses observed at the moderate dose, including the mucus secretory program. Moreover, the higher OE dose significantly increased the MUC5AC/MUC5B gel-forming mucin expression ratio and strongly downregulated ciliated cell expression programs, including key ciliating cell transcription factors (FOXJ1, MCIDAS). Our results suggest organic chemicals in PM2.5 likely drive cellular remodeling of the airway epithelium, punctuated by mucus metaplasia and loss of ciliated cells. This epithelial remodeling may underlie poor respiratory outcomes associated with high PM2.5 exposure.
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Project description:Development of Xenopus Mucociliary Epithelium
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Project description:Background: Whereas cilia damage and reduced cilia beat frequency have been implicated as causative of reduced mucociliary clearance in smokers, theoretically mucociliary clearance could also be affected by cilia length. Based on models of mucociliary clearance predicting cilia length must exceed the 6 -7 μm airway surface fluid depth to generate force in the mucus layer, we hypothesized cilia height may be decreased in airway epithelium of normal smokers compared to nonsmokers. Methodology/Principal Findings: Cilia length in normal nonsmokers and smokers was evaluated in aldehyde-fixed, paraffin-embedded endobronchial biopsies, and air-dried and hydrated samples brushed from human airway epithelium via fiberoptic bronchoscopy. In 28 endobronchial biopsies, healthy smoker cilia length was reduced 15% compared to nonsmokers (p<0.05). In 47 air-dried samples of airway epithelial cells, smoker cilia length was reduced 13% compared to nonsmokers (p<0.0001). Analysis of the length of individual, detached cilia in 17 samples, smoker cilia length was reduced 9% compared to nonsmokers (p<0.05). Finally, in 16 fully hydrated, unfixed samples, smoker cilia length was reduced 7% compared to nonsmokers (p<0.05). Conclusions/significance: Models predict that a reduction in cilia length would reduce mucociliary clearance, suggesting that smoking-associated shorter airway epithelial cilia plays a significant role in the pathogenesis of smoking-induced lung disease.
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