E-cigarette use increases susceptibility to bacterial infection by impairment of human neutrophil chemotaxis, phagocytosis, and NET formation.

Introduction:
This article explores the impact of e-cigarette vapor exposure on key neutrophil functions and the effects of chronic e-cigarette use on extravasation and chemotaxis of neutrophils in an infected space, and bacterial burden, following intraperitoneal challenge with P. aeruginosa. The study highlights the potential risks and consequences of e-cigarette use on the human immune system.

Key Points:

* The study used human neutrophils isolated from volunteers and exposed them to e-cigarette vapor extract (EVE).
* EVE exposure reduced chemotaxis, reactive oxygen species (ROS) production, and neutrophil extracellular trap (NET) formation in human neutrophils.
* Non-nicotine E-liquid formulations also inhibited NET production.
* Exposure to e-cigarette vapor daily for 1 month leads to systemic alterations in host defenses with diminished recruitment of murine neutrophils to the site of bacterial infection.
* E-cigarette-exposed mice had a higher burden of Pseudomonas intraperitoneally compared with air controls.
* The study used a combination of in vitro and in vivo models to assess the effects of e-cigarette vapor exposure on neutrophil function.
* The study highlights the potential risks and consequences of e-cigarette use on the human immune system.

Main Message:
The study provides compelling evidence that e-cigarette use adversely impacts the innate immune system, specifically by impairing key neutrophil functions. The findings suggest that e-cigarette users may be at higher risk for dysregulated inflammatory responses and invasive bacterial infections. Therefore, it is crucial to consider the potential immune-related risks associated with e-cigarette use and to communicate these risks effectively to the public.

Corriden R, Moshensky a, Bojanowski CM, et al. E-cigarette use increases susceptibility to bacterial infection by impairment of human neutrophil chemotaxis, phagocytosis, and NET formation. american journal of physiology Cell physiology. 2020;318(1):C205-C214. doi:10.1152/ajpcell.00045.2019