Comparison of electronic cigarette vs. cigarette smoke extract on macrophage function

Electronic cigarettes (e-cigs) are used as smoking cessation tools, but limited data exist on their biological effects. Chronic tobacco smoking alters macrophage (Mφ) function, resulting in impaired phagocytosis and altered cytokine release; it is possible that e-cigs similarly affect Mφ function. This study compared the effects of e-cigs compared to cigarettes on Mφ function. Six e-cigs (tobacco flavoured ± nicotine, banoffee pie flavoured ± nicotine, vehicle, or nicotine + vehicle) or 1 cigarette were 'smoked' for 2.5 min into media to generate e-cig vapour extract (e-CVE) or cigarette smoke extract (CSE). Monocyte-derived Mφ (N=6) cultured from healthy volunteers, were incubated for 24h with e-CVE or CSE, incubated for 4h with fluorescently-labelled <i>H.influenzae</i> or <i>S.pneumoniae</i>, and phagocytosis measured fluorimetrically, and TNFα, CXCL8 and IL-6 by ELISA. Expression of toll-like receptors (TLR)-2 and -4, and MARCO were measured by flow cytometry and cell viability by MTT assay. Neither CSE nor e-CVE affected cell viability or altered phagocytosis, though higher concentrations of CSE tended towards reduced phagocytosis. TNFα release was significantly reduced by CSE (72±4%, p&lt;0.05), 0% and 2.4% tobacco-flavoured e-CVE (44±14%, 37±9%, p&lt;0.05) and 0% and 2.4% banoffee pie flavoured e-CVE (44±14%, 55±17%, p&lt;0.05) whereas nicotine and vehicle had no effect. No effect was seen on CXCL8 or IL-6 release, expression of MARCO or on TLR2 and TLR4 expression. Flavoured e-CSE caused similar changes to Mφ cytokine release as CSE. E-CSE vehicle and nicotine alone had no effect, suggesting a constituent of flavourings are inhibitory. This hightlights the need for further study of e-cigs on lung health.