RESUMO
Clinical cases and experimental evidence revealed that electronic cigarettes (ECIG) induce serious adverse health effects, but underlying mechanisms remain to be fully uncovered. Based on recent exploratory evidence, investigating the effects of ECIG on macrophages can broadly define potential mechanisms by focusing on the effect of ECIG exposure with or without nicotine. Here we investigated the effect of ECIG-aerosol exposure on macrophages (MQ) phenotype, inflammatory response, and function of macrophages.MQ were cultured at air liquid interface and exposed to ECIG-aerosol. Oxidative stress was determined by reactive oxygen species (ROS), heat shock protein 60 (HSP60), glutathione peroxidase (GPx) and heme oxygenase1 (HMOX1). Lipid accumulation and lipid peroxidation were defined by lipid staining and level of malondialdehyde (MDA) respectively. MQ polarization was identified by surface expression markers CD86, CD11C and CD206 as well as pro-inflammatory and anti-inflammatory cytokines in gene and protein level. Phagocytosis of E. coli by MQ was investigated by fluorescence-based phagocytosis assay.ECIG-aerosol exposure in presence or absence of nicotine induced oxidative stress evidenced by ROS, HSP60, GPx, GPx4 and HMOX1 upregulation in MQ. ECIG-aerosol exposure induced accumulation of lipids and the lipid peroxidation product MDA in MQ. Pro-inflammatory MQ (M1) markers CD86 and CD11C but not anti-inflammatory MQ (M2) marker CD206 were upregulated in response to ECIG-aerosol exposure. In addition, ECIG induced pro-inflammatory cytokines IL-1beta and IL-8 in gene level and IL-6, IL-8, and IL-1beta in protein level whereas ECIG exposure downregulated anti-inflammatory cytokine IL-10 in protein level. Phagocytosis activity of MQ was downregulated by ECIG exposure. shRNA mediated lipid scavenger receptor 'CD36' silencing inhibited ECIG-aerosol-induced pro-inflammatory MQ polarization and recovered phagocytic activity of MQ.ECIG exposure alters lung lipid homeostasis and thus induced inflammation by inducing M1 type MQ and impair phagocytic function, which could be a potential cause of ECIG-induced lung inflammation in healthy and inflammatory exacerbation in disease condition.
RESUMO
Despite the growing popularity of electronic cigarettes (e-cigarettes) over the last decade, few epidemiological studies have examined the influence on respiratory health in young adulthood. The aim of this study was to identify factors associated with e-cigarette use in young adulthood in Sweden, and to examine associations between e-cigarette use and lung function, respiratory symptoms, and obesity. This cross-sectional study included 3055 young adults from Sweden and used questionnaire and clinical data obtained at age 22-25 years. The prevalence of current e-cigarette use was 3.9% (n = 120). Few participants reported daily (0.4%) or exclusive (0.8%) use of e-cigarettes. In a multivariable adjusted logistic regression model, e-cigarette use was significantly associated with male gender (OR:3.2; 95% CI:1.5-6.7) and cigarette smoking (OR:14.7; 95% CI:5.5-39.0 for daily smoking). Prevalence of cough (15.0% vs. 8.5%) and mucus production (22.3% vs. 14.8%) was significantly higher among e-cigarette users compared to non-users, while no difference in lung function was observed. In addition, the prevalence of overweight/obesity was higher among e-cigarette users compared to non-users (36.7% vs. 22.3% with BMI≥25 kg/m2). In conclusion, cigarette smokers and males used e-cigarette more often compared to females and non-cigarette smokers. Attention should be given to respiratory symptoms among e-cigarette users, although our results may be explained by the concurrent use of conventional cigarettes, as the group of exclusive e-cigarette users were too small to allow firm conclusions.
