Abstract:
BACKGROUND : Electronic cigarettes (ECs) are electronic aerosol delivery systems composed of nicotine and
various chemicals, which are widely used to facilitate smoking cessation. Although ECs are considered
safer than cigarettes, they do, however, contain chemical toxicants, some of which may interact with cells
of the host’s innate immune system of which neutrophils constitute a key component.
METHODS : The current study was designed to compare the effects of aqueous EC aerosol extracts (ECEs;
with or without nicotine) with those of cigarette smoke extract (CSE) on neutrophil and platelet reactivity
in vitro. Neutrophil reactivity is characterised by the generation of reactive oxygen species (ROS),
degranulation (elastase release) and the release of extracellular DNA (neutrophil extracellular trap (NET)
formation: NETosis), which were measured using chemiluminescence, spectrophotometric and microscopic
procedures, respectively. Platelet reactivity was measured according to the magnitude of upregulated
expression of the adhesion molecule CD62P on activated cells using a flow cytometric procedure.
RESULTS : Exposure of neutrophils to either ECEs or CSE caused a significant inhibition of ROS generation
and elastase release by N-formyl-L-methionyl-L-leucyl-L-phenylalanine (1 μM)-activated neutrophils. Pretreatment
of neutrophils with CSE also resulted in a marked attenuation of phorbol 12-myristate 13-acetate
(6.25 nM)-mediated release of extracellular DNA, which was unaffected by the ECEs. Similarly, CSE, but
not the ECEs, inhibited the expression of CD62P by platelets activated with ADP (100 μM).
CONCLUSIONS : These observations suggest that ECE aerosols may inhibit some of the immuno-protective
activities of neutrophils such as ROS production and elastase release by activated cells, the effect of which
was not enhanced by inclusion of nicotine. The inhibitory effects of CSE were significantly more
pronounced than those of ECEs, especially so for suppression of NET formation and platelet activation. If
operative in vivo, these harmful immunosuppressive effects of ECEs may compromise intrinsic pulmonary
antimicrobial defence mechanisms, albeit less so than cigarette smoke.
