Journal of Molecular Medicine

, Volume 94, Issue 6, pp 667–679

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

Authors

  • John H. Hwang
    • Pulmonary and Critical Care SectionVA San Diego Healthcare System
    • Department of Medicine, Division of Pulmonary and Critical CareUniversity of California at San Diego (UCSD)
  • Matthew Lyes
    • Pulmonary and Critical Care SectionVA San Diego Healthcare System
    • Duke University School of Medicine
  • Katherine Sladewski
    • Pulmonary and Critical Care SectionVA San Diego Healthcare System
  • Shymaa Enany
    • Microbiology and Immunology Department, Faculty of PharmacySuez Canal University
    • Pulmonary and Critical Care SectionVA San Diego Healthcare System
  • Elisa McEachern
    • Pulmonary and Critical Care SectionVA San Diego Healthcare System
    • Weill Cornell Medical College
  • Denzil P. Mathew
    • Pulmonary and Critical Care SectionVA San Diego Healthcare System
  • Soumita Das
    • Departments of Pathology and MedicineUCSD
  • Alexander Moshensky
    • Pulmonary and Critical Care SectionVA San Diego Healthcare System
  • Sagar Bapat
    • Salk Institute for Biological Studies
  • David T. Pride
    • Departments of Pathology and MedicineUCSD
  • Weg M. Ongkeko
    • Division of Head and Neck Surgery, Department of SurgeryUCSD
    • Pulmonary and Critical Care SectionVA San Diego Healthcare System
    • Department of Medicine, Division of Pulmonary and Critical CareUniversity of California at San Diego (UCSD)
Original Article

DOI: 10.1007/s00109-016-1378-3

Cite this article as:
Hwang, J.H., Lyes, M., Sladewski, K. et al. J Mol Med (2016) 94: 667. doi:10.1007/s00109-016-1378-3

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 vaporStaphylococcal virulenceCytotoxicityInflammatory lung diseaseAntimicrobial peptide LL-37MRSA pneumonia

Supplementary material

109_2016_1378_MOESM1_ESM.pdf (1017 kb)
ESM 1(PDF 0.99 mb)

Copyright information

© Springer-Verlag Berlin Heidelberg (outside the USA) 2016