Immunological and pathological effects of electronic cigarettes

Chen, I‐Ling; Todd, Ian; Fairclough, Lucy

doi:10.1111/bcpt.13225

Cited by 13 publications

(10 citation statements)

References 108 publications

(227 reference statements)

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“…Thus, EC are currently accepted as a healthier alternative to ordinary cigarettes [ 1 ]. While long-term effects of EC in people are not known, animal studies have demonstrated that there are toxic effects of EC [ 2 , 3 ], and in vitro studies have found some dysregulation in bronchial and lung epithelial cells, lung fibroblast, and alveolar macrophages [ 2 ].…”

Section: Introductionmentioning

confidence: 99%

Effect of sub-chronic exposure to cigarette smoke, electronic cigarette and waterpipe on human lung epithelial barrier function

et al. 2020

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Background Taking into consideration a recent surge of a lung injury condition associated with electronic cigarette use, we devised an in vitro model of sub-chronic exposure of human bronchial epithelial cells (HBECs) in air-liquid interface, to determine deterioration of epithelial cell barrier from sub-chronic exposure to cigarette smoke (CS), e-cigarette aerosol (EC), and tobacco waterpipe exposures (TW). Methods Products analyzed include commercially available e-liquid, with 0% or 1.2% concentration of nicotine, tobacco blend (shisha), and reference-grade cigarette (3R4F). In one set of experiments, HBECs were exposed to EC (0 and 1.2%), CS or control air for 10 days using 1 cigarette/day. In the second set of experiments, exposure of pseudostratified primary epithelial tissue to TW or control air exposure was performed 1-h/day, every other day, until 3 exposures were performed. After 16–18 h of last exposure, we investigated barrier function/structural integrity of the epithelial monolayer with fluorescein isothiocyanate–dextran flux assay (FITC-Dextran), measurements of trans-electrical epithelial resistance (TEER), assessment of the percentage of moving cilia, cilia beat frequency (CBF), cell motion, and quantification of E-cadherin gene expression by reverse-transcription quantitative polymerase chain reaction (RT-qPCR). Results When compared to air control, CS increased fluorescence (FITC-Dextran assay) by 5.6 times, whereby CS and EC (1.2%) reduced TEER to 49 and 60% respectively. CS and EC (1.2%) exposure reduced CBF to 62 and 59%, and cilia moving to 47 and 52%, respectively, when compared to control air. CS and EC (1.2%) increased cell velocity compared to air control by 2.5 and 2.6 times, respectively. The expression of E-cadherin reduced to 39% of control air levels by CS exposure shows an insight into a plausible molecular mechanism. Altogether, EC (0%) and TW exposures resulted in more moderate decreases in epithelial integrity, while EC (1.2%) substantially decreased airway epithelial barrier function comparable with CS exposure. Conclusions The results support a toxic effect of sub-chronic exposure to EC (1.2%) as evident by disruption of the bronchial epithelial cell barrier integrity, whereas further research is needed to address the molecular mechanism of this observation as well as TW and EC (0%) toxicity in chronic exposures.

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Section: Introductionmentioning

confidence: 99%

Effect of sub-chronic exposure to cigarette smoke, electronic cigarette and waterpipe on human lung epithelial barrier function

et al. 2020

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“…a means that assists smokers in their cessation efforts (Alzahrani, Pena, Temesgen, & Glantz, 2018). eCigs are hand-held electronic devices that generate vapors or aerosols from e-cigarette liquid (eCig liquid) without combustion (Chen, Todd, & Fairclough, 2019). eCig liquid usually contains a mixture of propylene glycol, glycerin, nicotine, and flavors (Alzahrani et al, 2018;Uchiyama et al, 2016).…”

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confidence: 99%

Cell invasion, RAGE expression, and inflammation in oral squamous cell carcinoma (OSCC) cells exposed to e‐cigarette flavoring

Tsai

Budge

Lepre

et al. 2020

Clinical & Exp Dental Res

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Objective Electronic cigarettes have given rise to a new, largely unregulated market within the smoking industry. While generally supposed to be less harmful than traditional tobacco smoke, awareness of the biological effects of electronic cigarette liquid is still scarce. Our objective was to determine the impact of electronic cigarette flavoring and nicotine on gingival squamous cell carcinoma invasion, RAGE expression, and the elaboration of pro‐inflammatory molecules. Methods and Materials Gingival and tongue squamous cell carcinoma cells were exposed to Red Hot or Green Apple flavored electronic cigarette flavoring with or without nicotine. Immunofluorescence determined RAGE expression. Real‐time cellular invasion was assessed using a RTCA DP instrument. Culture medium was assayed for cytokine secretion. Results Compared to controls we observed: increased cell invasion in gingival cells with Red Hot electronic cigarette flavoring and decreased cell invasion with Green Apple; decreased cell invasion in tongue cells treated with Red Hot electronic cigarette flavoring and no differences in invasion with Green Apple; flavor and nicotine dependent increases in RAGE expression; and differential expression of IL‐1α, IL‐8, and MMP‐13. Conclusion We conclude that electronic cigarette flavoring and nicotine orchestrate differential regulation of oral squamous cell carcinoma (OSCC) cell invasion and inflammatory effects. This study provides an important initial step in dissecting RAGE‐mediated mechanisms of cancerous invasion and molecular avenues employed by OSCC.

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“…(Nair et al 2019)]. Some flavourings have been shown to induce alterations in various cell types, including affecting their viability, proliferation, phagocytic ability and cytokine production (Chen et al 2019). It would there be of interest to use flavoured E-liquids to generate ECVE and evaluate their effects on DCs.…”

Section: Discussionmentioning

confidence: 99%

“…Although some studies have reported that CS and ECV have similar effects on various cell types (Chen et al 2019), others have found that the effects of CS are much more pronounced and deleterious than those of ECV (Husari et al 2016;Iskandar et al 2019;Taylor et al 2016). Therefore, in view of the critical role of DCs in immunity and the marked effects of CS on DCs, in the current study, the effects of ECV on the phenotype and function of DCs was investigated by creating an in vitro cell culture model using human moDCs.…”

Section: Introductionmentioning

confidence: 96%

“…Although it is still too soon to know the effects of chronic E-cigarette use over a period of decades, there have been several reports since 2014 of acute lung injury, pneumonitis and/or pneumonia associated with E-cigarette use (Arter et al 2019;Khan et al 2018;Layden et al 2019;Moore 2015;Nair et al 2019;Sommerfeld et al 2018;Thota and Latham 2014). E-cigarettes have been found to have effects on a variety of cell types in humans, including epithelial and endothelial cells, fibroblasts, macrophages and neutrophils (Chen et al 2019). However, the effects of E-cigarette vapours (ECV) on human myeloid DCs (mDCs) have not been studied previously.…”

Section: Introductionmentioning

confidence: 99%

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Electronic cigarette vapour moderately stimulates pro-inflammatory signalling pathways and interleukin-6 production by human monocyte-derived dendritic cells

et al. 2020

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Dendritic cells (DCs) are professional antigen presenting cells that play a critical role in bridging innate and adaptive immunity. Numerous studies have shown that tobacco constituents present in conventional cigarettes affect the phenotype and function of DCs; however, no studies have examined the effects of vapour from E-cigarettes on human DCs. Here, the effects of E-cigarette vapour extract (ECVE) on the phenotype and function of DCs were investigated by creating an in vitro cell culture model using human monocyte-derived DCs (MoDCs). Immature DCs were generated from peripheral blood monocytes and mature DCs were then produced by treatment with LPS or Poly I:C for 24 h. For LPS-matured DCs, 3% ECVE treatment slightly suppressed HLA-DR and CD86 expression, whereas 1% ECVE treatment enhanced IL-6 production. The overall expression of 29 signalling molecules and other cytoplasmic proteins (mainly associated with DC activation) was significantly upregulated in immature DCs by 1% ECVE, and in LPS-treated DCs by 3% ECVE. In particular, the condition that induced IL-6 production also upregulated MAPK pathway activation. These findings indicate that E-cigarette vapour moderately affects human DCs, but the effects are less pronounced than those reported for tobacco smoke.

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Immunological and pathological effects of electronic cigarettes

Cited by 13 publications

References 108 publications

Effect of sub-chronic exposure to cigarette smoke, electronic cigarette and waterpipe on human lung epithelial barrier function

Effect of sub-chronic exposure to cigarette smoke, electronic cigarette and waterpipe on human lung epithelial barrier function

Cell invasion, RAGE expression, and inflammation in oral squamous cell carcinoma (OSCC) cells exposed to e‐cigarette flavoring

Electronic cigarette vapour moderately stimulates pro-inflammatory signalling pathways and interleukin-6 production by human monocyte-derived dendritic cells

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