Electronic cigarette inhalation alters innate immunity and airway cytokines while increasing the virulence of colonizing bacteria

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 be toxic to airway cells, suppress host defenses, and promote inflammation over time, while also promoting virulence of colonizing bacteria.