Electronic cigarette vapour increases virulence and inflammatory potential of respiratory pathogens

Respir Res. 2019 Dec 18;20(1):267. doi: 10.1186/s12931-019-1206-8.

Abstract

Introduction: Bacteria have been extensively implicated in the development of smoking related diseases, such as COPD, by either direct infection or bacteria-mediated inflammation. In response to the health risks associated with tobacco exposure, the use of electronic cigarettes (e-cigs) has increased. This study compared the effect of e-cig vapour (ECV) and cigarette smoke (CSE) on the virulence and inflammatory potential of key lung pathogens (Haemophilus influenzae, Streptococcus pneumoniae, Staphylococcus aureus and Pseudomonas aeruginosa).

Methods: Biofilm formation, virulence in the Galleria mellonella infection model, antibiotic susceptibility and IL-8/TNF-α production in A549 cells, were compared between bacteria exposed to ECV, CSE and non-exposed bacteria.

Results: Statistically significant increases in biofilm and cytokine secretion were observed following bacterial exposure to either ECV or CSE, compared to non-exposed bacteria; the effect of exposure to ECV on bacterial phenotype and virulence was comparable, and in some cases greater, than that observed following CSE exposure. Treatment of A549 cells with cell signaling pathway inhibitors prior to infection, did not suggest that alternative signaling pathways were being activated following exposure of bacteria to either ECV or CSE.

Conclusions: These findings therefore suggest that ECV and CSE can induce changes in phenotype and virulence of key lung pathogens, which may increase bacterial persistence and inflammatory potential.

Keywords: Cigarette; Cytokine; E-cigarette; Inflammation; Lung; Pathogen; Persistence; Virulence.

Publication types

  • Comparative Study

MeSH terms

  • A549 Cells
  • Animals
  • Biofilms / drug effects*
  • Biofilms / growth & development
  • E-Cigarette Vapor / toxicity*
  • Haemophilus influenzae / drug effects*
  • Haemophilus influenzae / growth & development
  • Haemophilus influenzae / pathogenicity
  • Humans
  • Inflammation Mediators / metabolism
  • Interleukin-8 / metabolism
  • Larva / microbiology
  • Lung / drug effects*
  • Lung / metabolism
  • Lung / microbiology
  • Moths / embryology
  • Moths / microbiology
  • Nicotiana / adverse effects*
  • Pneumonia, Bacterial / chemically induced*
  • Pneumonia, Bacterial / metabolism
  • Pneumonia, Bacterial / microbiology
  • Pseudomonas aeruginosa / drug effects*
  • Pseudomonas aeruginosa / growth & development
  • Pseudomonas aeruginosa / pathogenicity
  • Smoke / adverse effects*
  • Staphylococcus aureus / drug effects*
  • Staphylococcus aureus / growth & development
  • Staphylococcus aureus / pathogenicity
  • Streptococcus pneumoniae / drug effects*
  • Streptococcus pneumoniae / growth & development
  • Streptococcus pneumoniae / pathogenicity
  • Tumor Necrosis Factor-alpha / metabolism
  • Virulence

Substances

  • CXCL8 protein, human
  • E-Cigarette Vapor
  • Inflammation Mediators
  • Interleukin-8
  • Smoke
  • TNF protein, human
  • Tumor Necrosis Factor-alpha