| Literature DB >> 29940344 |
Pranav Vasanthi Bathrinarayanan1, James E P Brown2, Lindsay J Marshall3, Laura J Leslie4.
Abstract
Currently there is a lack of consensus on the possible adverse health effects of E-cigarettes (ECs). Important factors including cell model employed and exposure method determine the physiological relevance of EC studies. The present study aimed to evaluate EC cytotoxicity using a physiologically relevant in-vitro multicellular model of human airways. Human bronchial epithelial cells (CALU-3) and pulmonary fibroblasts (MRC-5) were co-cultured at air-liquid-interface for 11-14 days post which they were exposed to whole cigarette smoke (WCS) or EC vapour (ECV) at standard ISO-3308 regime for 7 m using a bespoke aerosol delivery system. ECV effects were further investigated at higher exposure times (1 h-6 h). Results showed that while WCS significantly reduced cell viability after 7 m, ECV decreased cell viability only at exposure times higher than 3 h. Furthermore, ECV caused elevated IL-6 and IL-8 production despite reduced cell viability. ECV exposure also produced a marked increase in oxidative stress. Finally, WCS but not ECV exposure induced caspase 3/7 activation, suggesting a caspase independent death of ECV exposed cells. Overall, our results indicate that prolonged ECV exposure (≥3 h) has a significant impact on pro-inflammatory mediators' production, oxidative stress and cell viability but not caspase 3/7 activity.Entities:
Keywords: CALU 3; Co-culture model; Cytotoxicity; E-cigarette; Human airways; In-vitro; Multi-cellular
Mesh:
Year: 2018 PMID: 29940344 DOI: 10.1016/j.tiv.2018.06.020
Source DB: PubMed Journal: Toxicol In Vitro ISSN: 0887-2333 Impact factor: 3.500