Effect of cigarette smoke extracts (CSE) and e-cigarette vapour extracts (ECVE) on the production of cytokines and chemokines in human airway smooth muscle cells (HASMCs)

Abstract

Background: Chronic obstructive pulmonary disease (COPD) is characterised by an inflammatory response in the airways to inhaled substances like cigarette smoke. It is known that CSE stimulates the production of a number of inflammatory cytokines and chemokines in HASMCs. E-cigarettes are used to aid smoking cessation but they may also have pro-inflammatory effects. However, the effect of ECVE on cytokine and chemokine production in HASMCs is unknown. This study aims to compare the effect of CSE and ECVE on the production of inflammatory cytokines and chemokines in HASMCs. Methods: CSE (from 2 cigarettes) and ECVE with and without nicotine (N-/N+) (from 6ml e-liquid, 0.24mg/ml nicotine) were prepared by bubbling cigarette smoke and e-cigarette vapour into 20ml of cell culture medium. Confluent and growth-arrested HASMCs were treated with CSE and ECVE for 24 h. Cytokines and chemokines in the medium were measured by ELISA. Cell viability was analysed by MTT assay. Results: 5% CSE and 10% ECVE (N-/N+) reduced HASMC cell viability. CSE (1, 2 and 3.5%) concentration-dependently induced the production of IL-5, IL-6, IL-8, IL-13, vascular endothelial growth factor (VEGF) and CCL2, but not CXCL-10 and RANTES. ECVE (1, 2.5 and 5%) only significantly induced the production of IL-13, but not the others. Conclusion: Our results suggest that cigarette smoke has a wider pro-inflammatory effect in the airway than E-cigarette vapor. The effect of ECVE (N-/N+) on the cytotoxicity and IL-13 production suggests that E-cigarette vapor, not the nicotine in E-cigarette liquid, is harmful to the airway and can also cause airway inflammation.