Original Article

Journal of Molecular Medicine

, Volume 94, Issue 6, pp 667-679

First online:

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

  • John H. HwangAffiliated withPulmonary and Critical Care Section, VA San Diego Healthcare SystemDepartment of Medicine, Division of Pulmonary and Critical Care, University of California at San Diego (UCSD)
  • , Matthew LyesAffiliated withPulmonary and Critical Care Section, VA San Diego Healthcare SystemDuke University School of Medicine
  • , Katherine SladewskiAffiliated withPulmonary and Critical Care Section, VA San Diego Healthcare System
  • , Shymaa EnanyAffiliated withMicrobiology and Immunology Department, Faculty of Pharmacy, Suez Canal UniversityPulmonary and Critical Care Section, VA San Diego Healthcare System
  • , Elisa McEachernAffiliated withPulmonary and Critical Care Section, VA San Diego Healthcare SystemWeill Cornell Medical College
  • , Denzil P. MathewAffiliated withPulmonary and Critical Care Section, VA San Diego Healthcare System
  • , Soumita DasAffiliated withDepartments of Pathology and Medicine, UCSD
  • , Alexander MoshenskyAffiliated withPulmonary and Critical Care Section, VA San Diego Healthcare System
  • , Sagar BapatAffiliated withSalk Institute for Biological Studies
    • , David T. PrideAffiliated withDepartments of Pathology and Medicine, UCSD
    • , Weg M. OngkekoAffiliated withDivision of Head and Neck Surgery, Department of Surgery, UCSD
    • , Laura E. Crotty AlexanderAffiliated withPulmonary and Critical Care Section, VA San Diego Healthcare SystemDepartment of Medicine, Division of Pulmonary and Critical Care, University of California at San Diego (UCSD) Email author 

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Abstract

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.

Key message

  • 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.

Keywords

E-cigarette vapor Staphylococcal virulence Cytotoxicity Inflammatory lung disease Antimicrobial peptide LL-37 MRSA pneumonia