Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of human airway epithelial cells in asthmatics, smokers and healthy controls

ABSTRACT: We collected airway epithelial brushings for microarray analysis from 42 asthmatics and two control groups â 28 healthy subjects and 16 smokers. A subgroup of 32 asthmatics completed a randomized placebo-controlled trial of fluticasone propionate in which collection of brushings was repeated after 1 week of treatment. Experiment Overall Design: 1) Comparison of gene expression in asthmatics to healthy controls Experiment Overall Design: 2) Comparison of smokers to healthy controls Experiment Overall Design: 3) Comparison of change in gene expression in the fluticasone treated group to the change in the placebo treated group

ORGANISM(S): Homo sapiens

SUBMITTER: Prescott Gurney Woodruff

PROVIDER: E-GEOD-4302 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Genome-wide profiling identifies epithelial cell genes associated with asthma and with treatment response to corticosteroids.

Woodruff Prescott G PG Boushey Homer A HA Dolganov Gregory M GM Barker Chris S CS Yang Yee Hwa YH Donnelly Samantha S Ellwanger Almut A Sidhu Sukhvinder S SS Dao-Pick Trang P TP Pantoja Carlos C Erle David J DJ Yamamoto Keith R KR Fahy John V JV

Proceedings of the National Academy of Sciences of the United States of America 20070926 40

Airway inflammation and epithelial remodeling are two key features of asthma. IL-13 and other cytokines produced during T helper type 2 cell-driven allergic inflammation contribute to airway epithelial goblet cell metaplasia and may alter epithelial-mesenchymal signaling, leading to increased subepithelial fibrosis or hyperplasia of smooth muscle. The beneficial effects of corticosteroids in asthma could relate to their ability to directly or indirectly decrease epithelial cell activation by inf ...[more]

PMID: 17898169

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Project description:Background: The first step in SARS-CoV-2 infection is binding of the virus to angiotensin converting enzyme 2 (ACE2) on the airway epithelium. Asthma affects over 300 million people world-wide, many of whom may encounter SARS-CoV-2. Epidemiologic data suggests that asthmatics who get infected may be at increased risk of more severe disease. Our objective was to assess whether maintenance inhaled corticosteroids (ICS), a major treatment for asthma, is associated with airway ACE2 expression in asthmatics. Methods: Large airway epithelium (LAE) of asthmatics treated with maintenance ICS (ICS+), asthmatics not treated with ICS (ICS-), and healthy controls (controls) was analyzed for expression of ACE2 and other coronavirus infection-related genes using microarrays. Results: AsResults: As a group, there was no difference in LAE ACE2 expression in all asthmatics vs controls. In contrast, subgroup analysis demonstrated that LAE ACE2 expression was higher in asthmatics ICS+ compared to ICS‾ and ACE2 expression was higher in male ICS+ compared to female ICS+ and ICS‾ of either sex. ACE2 expression did not correlate with serum IgE, absolute eosinophil level, or change in FEV1 in response to bronchodilators in either ICS- or ICS+. Conclusion: Airway ACE2 expression is increased in asthmatics on long-term treatment with ICS, an observation that should be taken into consideration when assessing the use of inhaled corticosteroids during the pandemic. a group, there was no difference in LAE ACE2 expression in all asthmatics vs controls. In contrast, subgroup analysis demonstrated that LAE ACE2 expression was higher in asthmatics ICS+ compared to ICS‾ and ACE2 expression was higher in male ICS+ compared to female ICS+ and ICS‾ of either sex. ACE2 expression did not correlate with serum IgE, absolute eosinophil level, or change in FEV1 in response to bronchodilators in either ICS- or ICS+. Conclusion: Airway ACE2 expression is increased in asthmatics on long-term treatment with ICS, an observation that should be taken into consideration when assessing the use of inhaled corticosteroids during the pandemic.

Project description:Background: Around 5% of children with asthma suffer from chronic symptoms and/or severe exacerbations despite extensive treatment. The causes of severe therapy-resistant childhood asthma are poorly understood. Objectives: To define global patterns of gene expression in severe therapy-resistant vs. controlled asthma and healthy controls. Methods: Children with severe, therapy-resistant (SA, n=20) and controlled asthma (CA, n=20) were identified from a Swedish nation-wide study including extensive clinical and immunological characterisation. In addition, healthy controls were recruited (Ctrl, n=19). White blood cells were isolated and the global transcriptome profile was characterised using the Affymetrix Human Gene ST 1.0 chip. Results: 1378 genes were differentially expressed in one or several of the CA vs. Ctrl, SA vs. CA or SA vs. Ctrl contrasts. A large number could uniquely differentiate the SA group from the CA (n=351 genes) and Ctrl (n=315) groups, whereas fewer genes differentiated the CA from the Ctrl group (n=149). Several non-coding RNAs were found up-regulated in SA compared to CA or Ctrl. Three significantly enriched KEGG pathways were represented; bitter taste transduction, TAS2Rs (up-regulated mostly in SA), natural killer cell mediated cytotoxicity (up-regulated in CA) and N-Glycan biosynthesis (down-regulated in SA). An unsupervised hierarchical clustering of the 1378 genes could crudely separate the SA, CA and Ctrl individuals. Conclusion: Our data indicate a separation in gene expression patterns between children with severe, therapy-resistant asthma and controlled persistent asthma, and suggest novel pathways characterizing the severe therapy-resistant asthma phenotype. The transcriptomes of 59 subjects were assayed on the Affymetrix Human Gene ST 1.0 expression array. All samples passed pre-hybridisation quality control. After pre-processing and quality control of the post-hybridised arrays, five samples were regarded as outliers and removed (ctrl 510, MA 248, SA 141, SA 261, SA 41). The remaining sample set of 17 severe asthmatics (SA), 19 mild asthmatics (MA) and 18 controls (ctrl) were used for down-stream analysis.

Dataset Information

Transcription profiling of human airway epithelial cells in asthmatics, smokers and healthy controls

Publications

Genome-wide profiling identifies epithelial cell genes associated with asthma and with treatment response to corticosteroids.

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