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Electronic cigarette vapour increases virulence and inflammatory potential of respiratory pathogens

Authors
  • Gilpin, Deirdre F.1
  • McGown, Katie-Ann1
  • Gallagher, Kevin1
  • Bengoechea, Jose1
  • Dumigan, Amy1
  • Einarsson, Gisli1
  • Elborn, J. Stuart1
  • Tunney, Michael M.1
  • 1 Queen’s University Belfast, 97 Lisburn Road, Belfast, Northern Ireland, BT9 7BL, UK , Belfast (United Kingdom)
Type
Published Article
Journal
Respiratory Research
Publisher
BioMed Central
Publication Date
Dec 18, 2019
Volume
20
Issue
1
Identifiers
DOI: 10.1186/s12931-019-1206-8
Source
Springer Nature
Keywords
License
Green

Abstract

IntroductionBacteria 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).MethodsBiofilm 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.ResultsStatistically 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.ConclusionsThese 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.

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