ArticleScientific reports2020
Intermittent exposure to whole cigarette smoke alters the differentiation of primary small airway epithelial cells in the air-liquid interface culture.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 77 citations in OpenAlex.
- Preclinical models of COPD: a state of the art review.The European respiratory journal · 2026Review
- Review
- Epithelial cells in chronic obstructive pulmonary disease exacerbations: Targets for lung repair.Pharmacological reviews · 2026Review
- Reimagining human-centric drug development with new approach methodologies.Science (New York, N.Y.) · 2026Review
- Characterizing airway epithelial cultures grown on permeable inserts with different pore densities.Physiological reports · 2026Article
- Smoking-induced dysregulation of transposable elements in the small airway epithelium.Respiratory research · 2026Article
- New approaches to uncover COPD pathobiology and develop therapies.JCI insight · 2026Review
- Ironing out COPD: ferroptosis-driven immune dysregulation, metabolic rewiring, and precision therapeutic opportunities.Frontiers in immunology · 2026Review
- Measurement of nitric oxide production in mouse tracheal epithelial cell cultures differentiated at the air liquid interface.bioRxiv : the preprint server for biology · 2025Article
- Protocol for differentiating primary human small airway epithelial cells at the air-liquid interface.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- JUNB O-GlcNAcylation-Mediated Promoter Accessibility of Metabolic Genes Modulates Distinct Epithelial Lineage in Pulmonary Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Quantitative adverse outcome pathway modeling for cigarette-smoke-induced airway mucus hypersecretion. Part 1: adverse-outcome-pathway-basedFrontiers in toxicology · 2025Article
- Gut virome alterations in patients with chronic obstructive pulmonary disease.Microbiology spectrum · 2024Article
- Alterations in the molecular control of mitochondrial turnover in COPD lung and airway epithelial cells.Scientific reports · 2024Article
- Challenges in current inhalable tobacco toxicity assessment models: A narrative review.Tobacco induced diseases · 2024Review
- Airway ciliated cells in adult lung homeostasis and COPD.European respiratory review : an official journal of the European Respiratory Society · 2023Review
- Key challenges for in vitro testing of tobacco products for regulatory applications: Recommendations for dosimetry.Drug testing and analysis · 2023Article
- Azithromycin ameliorated cigarette smoke-induced airway epithelial barrier dysfunction by activating Nrf2/GCL/GSH signaling pathway.Respiratory research · 2023Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cigarette smoke (CS) is the leading risk factor to develop COPD. Therefore, the pathologic effects of whole CS on the differentiation of primary small airway epithelial cells (SAEC) were investigated, using cells from three healthy donors and three COPD patients, cultured under ALI (air-liquid interface) conditions. The analysis of the epithelial physiology demonstrated that CS impaired barrier formation and reduced cilia beat activity. Although, COPD-derived ALI cultures preserved some features known from COPD patients, CS-induced effects were similarly pronounced in ALI cultures from patients compared to healthy controls. RNA sequencing analyses revealed the deregulation of marker genes for basal and secretory cells upon CS exposure. The comparison between gene signatures obtained from the in vitro model (CS vs. air) with a published data set from human epithelial brushes (smoker vs. non-smoker) revealed a high degree of similarity between deregulated genes and pathways induced by CS. Taken together, whole cigarette smoke alters the differentiation of small airway basal cells in vitro. The established model showed a good translatability to the situation in vivo. Thus, the model can help to identify and test novel therapeutic approaches to restore the impaired epithelial repair mechanisms in COPD, which is still a high medical need.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.