NIH Research Festival
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Despite the vast popularity of electronic cigarette (e-cigarette) vaping, studies on acute adverse effects in human and animal report discrepant results with a decrease, an increase or no change in inflammatory markers and other cardiopulmonary effects. Owing to these variabilities, it is necessary to characterize the effects of acute vaping in a clearly defined animal model. Using state-of-the art exposure system, C57BL/6 male and female mice were exposed 3 hours daily for 10 days to e-cigarette vapor containing propylene glycol, vegetable glycerin and nicotine. Lung gene expression and protein levels of multiple inflammatory cytokines and chemokines, including TNF-α and IL-1β were measured by qPCR and ELISA. Interestingly, male mice exhibited significantly more severe lung inflammation compared to their female counterparts. Flowcytometry data revealed infiltration of inflammatory cells, particularly macrophages, and histopathological analysis showed accumulation of these immune cells around bronchioles. In addition, acute exposure to e-cigarette caused notable lung dysfunction in male mice than the female equivalents, pointing towards the emergence of emphysema. A detailed cardiac hemodynamic analysis also done using echocardiography and invasive pressure–volume conductance catheter technique, the gold standard method to assess myocardial contractile function independent from loading conditions and heart rate. Surprisingly, our data revealed a profound systolic and diastolic cardiac dysfunction in exposed male mice. Gene expression of cardiac inflammatory mediators also showed mild but significant increase in some of the cytokines and chemokines. Collectively, this study establishes a model of acute vaping-induced pulmonary inflammation that is linked with cardiopulmonary dysfunction in sex-dependent manner.
Scientific Focus Area: Molecular Pharmacology
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