In the United States, the recent surge of electronic cigarette (e-cig) use has raised questions concerning the safety of these devices. This study seeks to assess the pro-inflammatory and cellular stress effects of the vaped humectants propylene glycol (PG) and glycerol (GLY) on airway epithelial cells (16HBE cells and differentiated human bronchial epithelial cells) with a newly developed aerosol exposure system. This system allows for chemical characterization of e-cig generated aerosol particles as well as in vitro exposures of 16HBE cells at an air–liquid interface to vaped PG and GLY aerosol. Our data demonstrate that the process of vaping results in the formation of PG- and GLY-derived oligomers in the aerosol particles. Our in vitro data demonstrate an increase in pro-inflammatory cytokines IL-6 and IL-8 levels in response to vaped PG and GLY exposures. Vaped GLY also causes an increase in cellular stress signals HMOX1, NQO1, and carbonylated proteins when the e-cig device is operated at high wattages. Additionally, we find that the exposure of vaped PG causes elevated IL-6 expression, while the exposure of vaped GLY increases HMOX1 expression in human bronchial epithelial cells when the device is operated at high wattages. These findings suggest that vaporizing PG and GLY results in the formation of novel compounds and the exposure of vaped PG and GLY are detrimental to airway cells. Since PG and/or GLY is universally contained in all e-cig liquids, we conclude that these components alone can cause harm to the airway epithelium.

In the U.S., millions of adults use electronic cigarettes (e-cigs), and a majority of these users are former or current cigarette smokers. It is unclear, whether prior smoking status affects biological responses induced by e-cigs. In this study, differentiated human nasal epithelial cells (hNECs) from non-smokers and smokers at air-liquid-interface were acutely exposed to the e-cig generated aerosols of humectants, propylene glycol (PG) and glycerol (GLY). Mucin levels were examined in the apical washes and cytokine levels were assessed in the basolateral supernatants 24 hours post-exposure. The aerosol from the GLY exposure increased Mucin 5, Subtype AC (MUC5AC) levels in the apical wash of hNECs from non-smokers, but not smokers. However, the aerosol from GLY induced pro-inflammatory responses in hNECs from smokers. We also exposed hNECs from non-smokers and smokers to e-cig generated aerosol from PG:GLY with freebase nicotine or nicotine salt. The PG:GLY with freebase nicotine exposure increased MUC5AC and Mucin 5, Subtype B (MUC5B) levels in hNECs from non-smokers, but the nicotine salt exposure did not. The PG:GLY with nicotine salt exposure increased pro-inflammatory cytokines in hNECs from smokers, which was not seen with the freebase nicotine exposure. Taken together these data indicate that the e-cig generated aerosols from the humectants, mostly GLY, and the type of nicotine used cause differential effects in airway epithelial cells from non-smokers and smokers. As e-cig use is increasing, it is important to understand that the biological effects of e-cig use are likely dependent on prior cigarette smoke exposure.

The gut microbiota is made up of trillions of microbial cells including bacteria, viruses, fungi, and other microbial bodies and is greatly involved in the maintenance of proper health of the host body. In particular, the gut microbiota has been shown to not only be involved in brain development but also in the modulation of behavior, neuropsychiatric disorders, and neurodegenerative diseases including Alzheimer’s disease. The precise mechanism by which the gut microbiota can affect the development of Alzheimer’s disease is unknown, but the gut microbiota is thought to communicate with the brain directly via the vagus nerve or indirectly through signaling molecules such as cytokines, neuroendocrine hormones, bacterial components, neuroactive molecules, or microbial metabolites such as short-chain fatty acids. In particular, interventions such as probiotic supplementation, fecal microbiota transfer, and supplementation with microbial metabolites have been used not only to study the effects that the gut microbiota has on behavior and cognitive function, but also as potential therapeutics for Alzheimer’s disease. A few of these interventions, such as probiotics, are promising candidates for the improvement of cognition in Alzheimer ’s disease and are the focus of this review.

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