JUUL e-liquid exposure elicits cytoplasmic Ca2+ responses and leads to cytotoxicity in cultured airway epithelial cells

Zhang, Rui; Jones, Myles M.; Dornsife, R E; Wu, Tongde; Sivaraman, Vijay; Tarran, Robert; Onyenwoke, Rob U.

doi:10.1016/j.toxlet.2020.11.017

Cited by 13 publications

(24 citation statements)

References 53 publications

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“…Our previous work (Ghosh et al, 2020;Zhang et al, 2020) as well as the work of others (Rowell et al, 2020) have implicated the potential role of increased intracellular Ca 2+ as the mechanism of e-liquid-induced cytotoxicity in vitro (Figure 1A). In particular, it has been questioned if e-liquids may activate endoplasmic reticulum (ER)-resident Ca 2+ release as the mechanism of toxicity (Ghosh et al, 2020).…”

Section: Modeling a Sars-like Infection In Vaping Primed Lungsmentioning

confidence: 77%

“…Our previous studies have evaluated the differences in toxicity of resting/“unvaped” e-liquids upon human pulmonary cells ( Zhang et al, 2020 ). Though our data demonstrated clear increased inflammatory responses and toxicity associated with the e-liquids, our more recent work attempts to evaluate e-liquids after the “vaping” process, that is, heating the e-liquid to aerosolize it into an inhalable vapor.…”

Section: Resultsmentioning

confidence: 99%

“…Our previous work also focused on the role of Ca 2+ signaling in E-Cig-related cytotoxicity in vitro ( Zhang et al, 2020 ). Therefore, we evaluated whether an antagonist for calcium signaling (2-APB) could alter the prognosis of the animals within our treatment groups.…”

Section: Discussionmentioning

confidence: 99%

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Vaping Exacerbates Coronavirus-Related Pulmonary Infection in a Murine Model

et al. 2021

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Though the current preponderance of evidence indicates the toxicity associated with the smoking of tobacco products through conventional means, less is known about the role of “vaping” in respiratory disease. “Vaping” is described as the use of electronic cigarettes (E-Cigarettes or E-Cigs), which has only more recently been available to the public (∼10 years) but has quickly emerged as a popular means of tobacco consumption worldwide. The World Health Organization (WHO) declared the SARS-CoV-2 outbreak as a global pandemic in March 2020. SARS-CoV-2 can easily be transmitted between people in close proximity through direct contact or respiratory droplets to develop coronavirus infectious disease 2019 (COVID-19). Symptoms of COVID-19 range from a mild flu-like illness with high fever to severe respiratory distress syndrome and death. The risk factors for increased disease severity remain unclear. Herein, we utilize a murine-tropic coronavirus (beta coronavirus) MHV-A59 along with a mouse model and measures of pathology (lung weight/dry ratios and histopathology) and inflammation (ELISAs and cytokine array panels) to examine whether vaping may exacerbate the pulmonary disease severity of coronavirus disease. While vaping alone did result in some noted pathology, mice exposed with intranasal vaped e-liquid suffered more severe mortality due to pulmonary inflammation than controls when exposed to coronavirus infection. Our data suggest a role for vaping in increased coronavirus pulmonary disease in a mouse model. Furthermore, our data indicate that disease exacerbation may involve calcium (Ca2+) dysregulation, identifying a potential therapeutic intervention.

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Section: Modeling a Sars-like Infection In Vaping Primed Lungsmentioning

confidence: 77%

Section: Resultsmentioning

confidence: 99%

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Vaping Exacerbates Coronavirus-Related Pulmonary Infection in a Murine Model

et al. 2021

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“…The recent literature has presented a convincing association between the use of either the traditional combustible cigarette or e-cigarette use/vaping, and Ca 2+ signaling and its dysregulation, which ultimately results in the cytotoxicity of pulmonary epithelia. In brief, we (and others) have utilized both in vitro and in vivo models to demonstrate that exposure to e-cigarette liquids (e-liquids, which are the actual products consumed during the vaping process) can elevate cytosolic Ca 2+ levels and result in significant cytotoxicity and/or pathology [ 3 , 5 , 6 , 7 , 8 ]. Indeed, while one study has demonstrated that Ca 2+ influx is diminished within the bronchial epithelia of traditional smokers, which is due to decreased ORAI3-dependent Ca 2+ mobilization [ 3 ], studies have also shown that certain e-liquid flavor combinations specifically increase cytosolic Ca 2+ levels within both the human bronchial epithelial cell line CALU-3 and primary-derived human bronchial epithelial cells.…”

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confidence: 99%

“…These latter observations correlate with increased cytotoxicity [ 5 ]. In addition, when using e-liquids previously demonstrated to significantly increase intracellular Ca 2+ levels, increased levels of the inflammatory cytokine IL-6 as well as apoptosis and cell death were observed in both CALU-3 cells and a 2nd human epithelial cell line, A549 [ 6 ]. More recently, using an established method to deliver vaped e-liquids, we evaluated the effects of vaping upon pulmonary e-cigarette exposure in vivo using a murine model.…”

mentioning

confidence: 99%