MicroRNA expression profiling defines the impact of electronic cigarettes on human airway epithelial cells

Solleti, Siva Kumar; Bhattacharya, Soumyaroop; Aḥmad, Auṣāf; Wang, Qian; Mereness, Jared A.; Rangasamy, Tirumalai; Mariani, Thomas J.

doi:10.1038/s41598-017-01167-8

Cited by 55 publications

(35 citation statements)

References 76 publications

(100 reference statements)

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“…Various pathways such as the phospholipid and fatty acid triacylglycerol metabolisms were significantly enriched after ECIG-exposure [24]. Another study investigated the micro RNA (miRNA) response and the exposure of differentiated airway epithelial cells with ECIG-vapor resulted in the upregulation of oxaidative stress genes [58]. ECIGs also modify the metabolome of epithelial cells and showing significant changes partially overlapping with the effect of TCIG [59].…”

Section: Resultsmentioning

confidence: 99%

Cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells

et al. 2020

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Background: The 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). Methods: We 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. Results: Bacterial 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. Conclusion: The 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. Background The contribution of exposure to cigarette smoke (CS) to the development and progression of chronic obstructive pulmonary disease (COPD), cancer, and cardiovascular diseases is widely recognized [1, 2]. Electronic cigarettes (ECIGs) are commercially available since 2004, but patents for similar devices reach back to 1965 [3, 4]. ECIGs are devices that produce a vapor by heating a liquid [3] that usually contains a mixture of glycerol, propylene-glycol, water, flavors, and different concentrations of nicotine. The flavors cover a broad range of tastes from fruit or spices, to different brands of tobacco. An intense scientific and political discussion about the toxicity and potential harm reduction of ECIGs is ongoing. Glycerol-propylene-glycol-water mixtures have been in use for a long time as artificial fog in aviation emergency training and entertainment business, but only a few studies about possible side effects exist before the emergence of ECIGs [5, 6]. Several studies have analyzed the effects of ECIGs on lung cells with the goal to evaluate toxic effects on cells and tissues [7]. A number of negative outcomes on different tissue culture systems (cell death, impaired repair, oxidative stress) have been reported [7-9]. In parallel, several ...

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Section: Resultsmentioning

confidence: 99%

Cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells

et al. 2020

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“…There is evidence from previous studies that ECV has the potential to induce oxidative stress in airway cells. For example, GOEL et al [23] reported that ECV contains up to 10×10 13 free radicals per puff [23], CARNEVALE et al [24] reported increased circulating oxidative stress markers in adults after vaping, and SOLLETI et al [25] reported that ECV is a potent inducer of oxidative stress response genes in bronchial epithelial cells in vitro. In the present study, the high OP of ECV, the presence in ECV of redox-promoting metals such as copper and iron, and attenuation of ECV-stimulated pneumococcal adhesion by the antioxidant N-acetyl cysteine, supports a role for oxidative stress as the initial stimulus for PAFR-dependent adhesion.…”

Section: Discussionmentioning

confidence: 99%

E-cigarette vapour enhances pneumococcal adherence to airway epithelial cells

et al. 2018

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E-cigarette vapour contains free radicals with the potential to induce oxidative stress. Since oxidative stress in airway cells increases platelet-activating factor receptor (PAFR) expression, and PAFR is co-opted by pneumococci to adhere to host cells, we hypothesised that E-cigarette vapour increases pneumococcal adhesion to airway cells.Nasal epithelial PAFR was assessed in non-vaping controls, and in adults before and after 5 min of vaping. We determined the effect of vapour on oxidative stress-induced, PAFR-dependent pneumococcal adhesion to airway epithelial cells , and on pneumococcal colonisation in the mouse nasopharynx. Elemental analysis of vapour was done by mass spectrometry, and oxidative potential of vapour assessed by antioxidant depletionThere was no difference in baseline nasal epithelial PAFR expression between vapers (n=11) and controls (n=6). Vaping increased nasal PAFR expression. Nicotine-containing and nicotine-free E-cigarette vapour increased pneumococcal adhesion to airway cells Vapour-stimulated adhesion was attenuated by the PAFR blocker CV3988. Nicotine-containing E-cigarette vapour increased mouse nasal PAFR expression, and nasopharyngeal pneumococcal colonisation. Vapour contained redox-active metals, had considerable oxidative activity, and adhesion was attenuated by the antioxidant N-acetyl cysteine.This study suggests that E-cigarette vapour has the potential to increase susceptibility to pneumococcal infection.

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“…In a recent study, Solleti et al demonstrated that smoking of electronic cigarettes affected the expression of 125 miRNAs (26). The present study systematically analyzed the expression patterns of miRNAs in nicotinetreated PDLCs.…”

Section: Discussionmentioning

confidence: 90%

MicroRNA expression profiling of nicotine-treated human periodontal ligament cells

Cheng

Zhao

et al. 2019

J Oral Sci

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Cigarette smoking is a lifestyle-related risk factor involved in the causation and progression of periodontal disease. Nicotine is a key toxic component of tobacco. However, the mechanisms underlying nicotine-induced periodontitis have not yet been fully elucidated. The present study investigated the microRNA (miRNA) expression profile of human periodontal ligament cells (PDLCs) treated with nicotine. Using differential analysis of miRNA array data, several differentially expressed miRNAs were identified in nicotine-treated PDLCs. Quantitative real-time PCR was employed to verify the accuracy of the miRNA array, and the targets of these dysregulated miRNAs were further analyzed. Function and pathway enrichment of differentially expressed miRNAs suggested that several important signaling pathways, such as the Toll-like receptor signaling pathway, nicotine addiction, the transforming growth factor-beta signaling pathway, and the hypoxia inducible factor-1 signaling pathway, are potentially responsible for nicotine-induced periodontitis. This study has helped to clarify the epigenetic mechanisms of nicotine-induced periodontitis, highlighting novel biomarkers and therapeutic targets.

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MicroRNA expression profiling defines the impact of electronic cigarettes on human airway epithelial cells

Cited by 55 publications

References 76 publications

Cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells

Cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells

E-cigarette vapour enhances pneumococcal adherence to airway epithelial cells

MicroRNA expression profiling of nicotine-treated human periodontal ligament cells

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