Hwang John H, Lyes Matthew, Sladewski Katherine, Enany Shymaa, McEachern Elisa, Mathew Denzil P, Das Soumita, Moshensky Alexander, Bapat Sagar, Pride David T, Ongkeko Weg M, Crotty Alexander Laura E
Pulmonary and Critical Care Section, VA San Diego Healthcare System, 3350 La Jolla Village Dr, MC 111J, San Diego, CA, 92161, USA.
Department of Medicine, Division of Pulmonary and Critical Care, University of California at San Diego (UCSD), La Jolla, CA, 92093, USA.
J Mol Med (Berl). 2016 Jun;94(6):667-79. doi: 10.1007/s00109-016-1378-3. Epub 2016 Jan 25.
Electronic (e)-cigarette use is rapidly rising, with 20 % of Americans ages 25-44 now using these drug delivery devices. E-cigarette users expose their airways, cells of host defense, and colonizing bacteria to e-cigarette vapor (EV). Here, we report that exposure of human epithelial cells at the air-liquid interface to fresh EV (vaped from an e-cigarette device) resulted in dose-dependent cell death. After exposure to EV, cells of host defense-epithelial cells, alveolar macrophages, and neutrophils-had reduced antimicrobial activity against Staphylococcus aureus (SA). Mouse inhalation of EV for 1 h daily for 4 weeks led to alterations in inflammatory markers within the airways and elevation of an acute phase reactant in serum. Upon exposure to e-cigarette vapor extract (EVE), airway colonizer SA had increased biofilm formation, adherence and invasion of epithelial cells, resistance to human antimicrobial peptide LL-37, and up-regulation of virulence genes. EVE-exposed SA were more virulent in a mouse model of pneumonia. These data suggest that e-cigarettes may be toxic to airway cells, suppress host defenses, and promote inflammation over time, while also promoting virulence of colonizing bacteria.
Acute exposure to e-cigarette vapor (EV) is cytotoxic to airway cells in vitro. Acute exposure to EV decreases macrophage and neutrophil antimicrobial function. Inhalation of EV alters immunomodulating cytokines in the airways of mice. Inhalation of EV leads to increased markers of inflammation in BAL and serum. Staphylococcus aureus become more virulent when exposed to EV.
电子烟的使用正在迅速增加，年龄在25至44岁的美国人中，现在有20%的人在使用这些药物输送装置。电子烟使用者会使他们的气道、宿主防御细胞和定植细菌暴露于电子烟烟雾（EV）中。在此，我们报告，在气液界面将人上皮细胞暴露于新鲜的电子烟烟雾（从电子烟装置中吸出）会导致剂量依赖性细胞死亡。暴露于电子烟烟雾后，宿主防御细胞——上皮细胞、肺泡巨噬细胞和中性粒细胞——对金黄色葡萄球菌（SA）的抗菌活性降低。小鼠每天吸入电子烟烟雾1小时，持续4周，导致气道内炎症标志物发生改变，血清中一种急性期反应物升高。暴露于电子烟烟雾提取物（EVE）后，气道定植菌金黄色葡萄球菌的生物膜形成增加、对上皮细胞的黏附和侵袭增强、对人抗菌肽LL-37的抗性增强以及毒力基因上调。在肺炎小鼠模型中，暴露于EVE的金黄色葡萄球菌毒力更强。这些数据表明，电子烟可能随着时间的推移对气道细胞有毒性、抑制宿主防御并促进炎症，同时还促进定植细菌的毒力。
急性暴露于电子烟烟雾（EV）在体外对气道细胞具有细胞毒性。急性暴露于EV会降低巨噬细胞和中性粒细胞的抗菌功能。吸入EV会改变小鼠气道中的免疫调节细胞因子。吸入EV会导致支气管肺泡灌洗（BAL）液和血清中炎症标志物增加。金黄色葡萄球菌暴露于EV后毒力增强。
