Electronic cigarette vapour increases virulence and inflammatory potential of respiratory pathogens

Deirdre F Gilpin,Gisli Einarsson,Michael M Tunney,Amy Dumigan,Jose Bengoechea,Kevin Gallagher,Katie-Ann Mcgown,J Stuart Elborn

doi:10.1186/s12931-019-1206-8

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.

Highlights

Bacteria have been extensively implicated in the development of smoking related diseases, such as chronic obstructive pulmonary disease (COPD), by either direct infection or bacteria-mediated inflammation
Determination of total viable count (TVC) of bacteria following growth in cigarette smoke extract (CSE) or e-cig vapour extract (ECVE) CSE or ECVE had no observable effect on the growth of any isolate tested, at any concentration, compared to growth of the isolate in media without CSE/ECVE. (Additional file 1: Figure S1)
Comparison of Transmission electron micrograph (TEM) images following exposure to either CSE or ECVE showed no gross physiological changes compared to bacteria grown in media alone, with the exception of P.aeruginosa

Summary

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). Exposure to cigarette smoke initiates a cascade of tissue inflammatory responses and protease imbalances, which contribute to lung inflammation and aid establishment of chronic lung infection [3,4,5]. Since e-cigs contain fewer toxic chemicals, and Bacteria, Haemophilus influenzae, Streptococcus pneumoniae, Staphylococcus aureus and Pseudomonas aeruginosa have all been implicated in the development of smoking-related chronic lung disease, through both direct infection and bacteria-mediated inflammation [14]. Sequencing based studies have shown that these bacteria are associated with the development of a lung community skewed towards loss of diversity, and associated with declining lung function [15, 16]

Methods

Results

Discussion

Conclusion