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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As electronic cigarette (E-cig) use, also known as “vaping”, has rapidly increased in popularity, data regarding potential pathologic effects are recently emerging. Recent associations between vaping and lung pathology have led to an increased need to scrutinize E-cigs for adverse health impacts. Our previous work (and others) has associated vaping with Ca2+-dependent cytotoxicity in cultured human airway epithelial cells. Herein, we develop a vaped e-liquid pulmonary exposure mouse model to evaluate vaping effects in vivo. Using this model, we demonstrate lung pathology through the use of preclinical measures, that is, the lung wet: dry ratio and lung histology/H&E staining. Further, we demonstrate that acute vaping increases macrophage chemotaxis, which was ascertained using flow cytometry-based techniques, and inflammatory cytokine production, via Luminex analysis, through a Ca2+-dependent mechanism. This increase in macrophage activation appears to exacerbate pulmonary pathology resulting from microbial infection. Importantly, modulating Ca2+ signaling may present a therapeutic direction for treatment against vaping-associated pulmonary inflammation.