Researchers at the VA San Diego Healthcare System (VASDHS) and the University of California, San Diego (UCSD), tested the effects of e-cigarette vapour on live methicillin-resistant Staphylococcus aureus (MRSA) and human epithelial cells.
MRSA commonly colonises the epithelium of the nasopharynx, where the bacteria and epithelial cells are exposed constantly to inhaled substances such as e-cigarette vapour and cigarette smoke.
"The virulence of MRSA is increased by e-cigarette vapour," said lead investigator Laura E Crotty Alexander.
Exposure to e-cigarette vapour increased the virulence of the bacteria, helping MRSA escape killing by antimicrobial peptides and macrophages.
However, she added, the vapour did not make the bacteria as aggressive as cigarette smoke exposure did in parallel studies her group conducted.
The researchers grew MRSA (USA 300 strain) in culture with vapour concentrations similar to inhalers on the market.
They looked at five factors that contribute to MRSA virulence: growth rate, susceptibility to reactive oxygen species (ROS), surface charge, hydrophobicity and biofilm formation.
In particular, e-cigarette vapour led to alterations in surface charge and biofilm formation, which conferred greater resistance to killing by human cells and antibiotics.
Alexander said that one possible contribution to the increased virulence of MRSA was the rapid change in pH induced by e-cigarette vapour.
Exposure changed the pH from 7.4 up to 8.4, making the environment very alkalotic for bacterial and mammalian cells.
This alkalosis stresses the cells, giving them a danger signal, leading to activation of defence mechanisms. The bacteria make their surface more positively charged, to avoid binding by the lethal antimicrobial peptides produced by human innate immune cells.
The bacteria also form thicker biofilms, increasing their stickiness and making MRSA less vulnerable to attack.
These changes make MRSA more virulent. But, when MRSA is exposed to regular cigarette smoke, their virulence is even greater.
Cigarette smoke induces surface charge changes 10-fold greater than that of e-cigarette exposure, alters hydrophobicity and decreases sensitivity to reactive oxygen species and antimicrobial peptides.
In a mouse model of pneumonia, cigarette smoke exposed MRSA had four-times greater survival in the lungs, and killed 30 per cent more mice than control MRSA. E-cigarette vapour exposed MRSA were also more virulent in mice, with a three-fold higher survival.