Electronic Cigarette Inhalation Alters Innate Immunity and Airway Cytokines While Increasing the Vir
Thursday, March 17, 2016
Posted by: Natalia Gromov
John H. Hwang, Matthew Lyes, Katherine Sladewski, Shymaa Enany, Elisa McEachern, Denzil P. Mathew, Soumita Das, Alexander Moshensky, Sagar Bapat, et al.
Electronic Cigarette Inhalation Alters Innate Immunity and Airway Cytokines While Increasing the Virulence of Colonizing Bacteria.
Journal of Molecular Medicine.First online: 25 January 2016. doi:10.1007/s00109-016-1378-3
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.