ArticleRespiratory research2020
Cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells.
Article in Respiratory research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Lung Damage Caused by Heated Tobacco Products and Electronic Nicotine Delivery Systems: A Systematic Review.International journal of environmental research and public health · 2021Pooled it
- Tobacco smoke but not e-cigarette vapor induces epithelial barrier disruption, inflammation, and DNA damage in human Calu-3 cells.Scientific reports · 2026Article
- Article
- The respiratory epithelium in the era of vaping: insights fromEuropean respiratory review : an official journal of the European Respiratory Society · 2025Review
- Protocol for differentiating primary human small airway epithelial cells at the air-liquid interface.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Open-source, three-dimensionally printed manifolds for exposure studies using human airway epithelial cells.ERJ open research · 2025Article
- Impact of electronic cigarettes (e-cigs) and heat-not-burn/heated tobacco products (HnB/HTP) on asthma and chronic obstructive pulmonary disease: a viewpoint of the Italian Society of Internal Medicine.Internal and emergency medicine · 2024Review
- Single-cell transcriptomics reveals e-cigarette vapor-induced airway epithelial remodeling and injury.Respiratory research · 2024Article
- Advances in non-type 2 severe asthma: from molecular insights to novel treatment strategies.The European respiratory journal · 2024Review
- Article
- Electronic cigarette exposure disrupts airway epithelial barrier function and exacerbates viral infection.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Transcriptomic responses in the blood and sputum of cigarette smokers compared to e-cigarette vapers.Respiratory research · 2023Article
- Pathogenesis of E-Cigarette Vaping Product Use-Associated Lung Injury (EVALI).Comprehensive Physiology · 2023Article
- Considerations on dosimetry for in vitro assessment of e-cigarette toxicity.Respiratory research · 2022Review
- Early transcriptional responses of bronchial epithelial cells to whole cigarette smoke mirror those of in-vivo exposed human bronchial mucosa.Respiratory research · 2022Article
- Propylene glycol, a component of electronic cigarette liquid, damages epithelial cells in human small airways.Respiratory research · 2022Article
- Electronic cigarette liquids impair metabolic cooperation and alter proteomic profiles in V79 cells.Respiratory research · 2022Article
- Predicting the pulmonary effects of long-term e-cigarette use: are the clouds clearing?European respiratory review : an official journal of the European Respiratory Society · 2022Review
- Fundamentals of vaping-associated pulmonary injury leading to severe respiratory distress.Life science alliance · 2022Article
- Human Bronchial Epithelial Cell Culture Models for Cigarette Smoke and Vaping Studies.Methods in molecular biology (Clifton, N.J.) · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe use of electronic cigarettes (ECIGs) is increasing, but the impact of ECIG-vapor on cellular processes like inflammation or host defense are less understood. The aim of the present study was to compare the acute effects of traditional cigarettes (TCIGs) and ECIG-exposure on host defense, inflammation, and cellular activation of cell lines and primary differentiated human airway epithelial cells (pHBE).
methodsWe exposed pHBEs and several cell lines to TCIG-smoke or ECIG-vapor. Epithelial host defense and barrier integrity were determined. The transcriptome of airway epithelial cells was compared by gene expression array analysis. Gene interaction networks were constructed and differential gene expression over all groups analyzed. The expression of several candidate genes was validated by qRT-PCR.
resultsBacterial killing, barrier integrity and the expression of antimicrobial peptides were not affected by ECIG-vapor compared to control samples. In contrast, TCIGs negatively affected host defense and reduced barrier integrity in a significant way. Furthermore ECIG-exposure significantly induced IL-8 secretion from Calu-3 cells but had no effect on NCI-H292 or primary cells. The gene expression based on array analysis distinguished TCIG-exposed cells from ECIG and room air-exposed samples.
conclusionThe transcriptome patterns of host defense and inflammatory genes are significantly distinct between ECIG-exposed and TCIG-treated cells. The overall effects of ECIGs on epithelial cells are less in comparison to TCIG, and ECIG-vapor does not affect host defense. Nevertheless, although acute exposure to ECIG-vapor induces inflammation, and the expression of S100 proteins, long term in vivo data is needed to evaluate the chronic effects of ECIG use.
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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.