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E-cigarettes compromise the gut barrier, trigger inflammation

ABSTRACT: Despite the rising popularity of e-cigarette and vaping devices, their safety continues to be questioned. Using established murine models of acute and chronic e-cigarette aerosol inhalation, murine colon transcriptomics and organoid co-culture models, here we assessed the effects of e-cigarette use on the gut barrier. Histologic and transcriptome analyses revealed that chronic, but not acute, nicotine-free e-cigarette use was associated with inflammation and reduced expression of tight junction markers, including occludin. Exposure of murine and human enteroid-derived monolayers (EDMs) to nicotine-free e-cigarette aerosols alone or in co-culture with invasive E. coli, recapitulated the key findings observed in vivo, i.e., barrier-disruption, downregulation of occludin, inflammation, and an accentuated risk of and response to bacterial infection. These data highlight an unexpected harmful effect of ecigarette use on the gut barrier and pinpoint non-nicotine chemical components as the source of harm. Considering the importance of an intact gut barrier for host fitness, and the impact of gut mucosal inflammation on a multitude of chronic diseases, these findings are broadly relevant to medicine and public health.

ORGANISM(S): Mus musculus

PROVIDER: GSE161521 | GEO | 2020/11/17

REPOSITORIES: GEO

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Electronic cigarette exposure disrupts blood-brain barrier integrity, promotes neuroinflammation, and leads to cognitive dysfunction

Project description:Electronic cigarette (EC) use has grown substantially since entry into the US market, particularly among adolescents and combustible tobacco users. Despite growing popularity and claims of harm reduction, the health effects of these products outside the lung is poorly understood. Several constituents of cigarette smoke (CS) with known neurovascular and inflammatory effects are present in EC liquids or formed during the generation of vapor. The present study characterizes the impact of EC exposure on neuroinflammation and blood-brain barrier (BBB) function, and provides comparison of outcomes with reference cigarette exposure normalized to comparable levels of nicotine delivery. Additionally, the contribution of nicotine to observed effects is elucidated through comparison with EC liquids which are verified to be nicotine-free. C57BL/6 mice are exposed to 2 hrs of daily EC vapor or CS, beginning at 8 wks of age. Changes in BBB gene expression are first characterized by whole exome sequencing of isolated brain microvessels following chronic (2 month) EC exposure.

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Opioid-induced gut microbial disruption leads to gut barrier compromise and sustained systemic inflammation.

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An application of a systems toxicology approach using a human organotypic small airway cultures for a comparative assessment between a candidate modified-risk tobacco product aerosol and cigarette smoke.

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