ArticlePloS one2011
Biologic phenotyping of the human small airway epithelial response to cigarette smoking.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed.
- Functional interactors of three genome-wide association study genes are differentially expressed in severe chronic obstructive pulmonary disease lung tissue.Scientific reports · 2017Trial
- Asthma-COPD overlap. Clinical relevance of genomic signatures of type 2 inflammation in chronic obstructive pulmonary disease.American journal of respiratory and critical care medicine · 2015Trial
- Identification ofInternational journal of chronic obstructive pulmonary disease · 2026Article
- Integrating bioinformatics and molecular experiments to reveal the critical role of the cellular energy metabolism-related marker PLA2G1B in COPD epithelial cells.Frontiers in immunology · 2025Article
- Deciphering the molecular regulatory of RAB32/GPRC5A axis in chronic obstructive pulmonary disease.Respiratory research · 2024Article
- Serial Sampling of the Small Airway Epithelium to Identify Persistent Smoking-dysregulated Genes.American journal of respiratory and critical care medicine · 2023Article
- Oxidised IL-33 drives COPD epithelial pathogenesisThe European respiratory journal · 2023Article
- Identifying chronic obstructive pulmonary disease from integrative omics and clustering in lung tissue.BMC pulmonary medicine · 2023Article
- Exploring the shared gene signatures of smoking-related osteoporosis and chronic obstructive pulmonary disease using machine learning algorithms.Frontiers in molecular biosciences · 2023Article
- A Single-Cell Atlas of Large and Small Airways at Birth in a Porcine Model of Cystic Fibrosis.American journal of respiratory cell and molecular biology · 2022Article
- Gene Expression Trajectories from Normal Nonsmokers to COPD Smokers and Disease Progression Discriminant Modeling in Response to Cigarette Smoking.Disease markers · 2022Article
- Bioinformatic Analysis ofMembranes · 2021Article
- Analysis of the polarization states of the alveolar macrophages in chronic obstructive pulmonary disease samples based on miRNA-mRNA network signatures.Annals of translational medicine · 2021Article
- Up-regulation of ACE2, the SARS-CoV-2 receptor, in asthmatics on maintenance inhaled corticosteroids.Respiratory research · 2021Article
- Cigarette Smoke Activates NOTCH3 to Promote Goblet Cell Differentiation in Human Airway Epithelial Cells.American journal of respiratory cell and molecular biology · 2021Article
- Expression of endocannabinoid system components in human airway epithelial cells: impact of sex and chronic respiratory disease status.ERJ open research · 2020Article
- Vitamin D Metabolism Is Dysregulated in Asthma and Chronic Obstructive Pulmonary Disease.American journal of respiratory and critical care medicine · 2020Article
- Expression of the SARS-CoV-2American journal of respiratory and critical care medicine · 2020Article
- Intermittent exposure to whole cigarette smoke alters the differentiation of primary small airway epithelial cells in the air-liquid interface culture.Scientific reports · 2020Article
- Association of Cigarette Smoking, COPD, and Lung Cancer With Expression of SARS-CoV-2 Entry Genes in Human Airway Epithelial Cells.Frontiers in medicine · 2020Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
backgroundThe first changes associated with smoking are in the small airway epithelium (SAE). Given that smoking alters SAE gene expression, but only a fraction of smokers develop chronic obstructive pulmonary disease (COPD), we hypothesized that assessment of SAE genome-wide gene expression would permit biologic phenotyping of the smoking response, and that a subset of healthy smokers would have a "COPD-like" SAE transcriptome. METHODOLOGY/PRINCIPAL
findingsSAE (10th-12th generation) was obtained via bronchoscopy of healthy nonsmokers, healthy smokers and COPD smokers and microarray analysis was used to identify differentially expressed genes. Individual responsiveness to smoking was quantified with an index representing the % of smoking-responsive genes abnormally expressed (I(SAE)), with healthy smokers grouped into "high" and "low" responders based on the proportion of smoking-responsive genes up- or down-regulated in each smoker. Smokers demonstrated significant variability in SAE transcriptome with I(SAE) ranging from 2.9 to 51.5%. While the SAE transcriptome of "low" responder healthy smokers differed from both "high" responders and smokers with COPD, the transcriptome of the "high" responder healthy smokers was indistinguishable from COPD smokers. CONCLUSION/SIGNIFICANCE: The SAE transcriptome can be used to classify clinically healthy smokers into subgroups with lesser and greater responses to cigarette smoking, even though these subgroups are indistinguishable by clinical criteria. This identifies a group of smokers with a "COPD-like" SAE transcriptome.
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