Effect of cigarette smoke extract on inflammatory cytokine and chemokine production in human airway smooth muscle cells

Abstract

<b>Background:</b> Asthma is associated with Th2-mediated eosinophilic airway inflammation. Whether cigarette smoke extract (CSE) can affect Th2 cytokine and eosinophil chemokine production in vitro remains unclear. This study examines the effect of CSE on the production of Th2 cytokines, eosinophil chemokines, and neutrophil chemoattractant IL-8 in human airway smooth muscle cells (HASMCs). <b>Methods:</b> CSE was prepared from the smoke of two cigarettes (3R4F) into 20 mL of cell culture medium. Confluent and serum-starved HASMCs were pre-treated with and without CSE (3.5%) for 24 h followed by incubation with CSE, TNFa (1ng/ml), or CSE+ TNFa for 24 h. Bio-Plex Pro™ Human Cytokine 27-plex Assay was used to measure the cytokines/chemokines in the collected medium. <b>Results:</b> CSE inhibited the production of Th2 cytokines (IL-4 and IL-13, IL-5 was not affected by CSE) and eosinophil chemokines (eotaxin, IP-10, and RANTES) but induced the production of the neutrophil chemoattractant IL-8 in HASMCs. TNFa alone induced the production of Th2 cytokines, eosinophil chemokines, and IL-8. Interestingly, CSE inhibited TNFα-induced the production of Th2 cytokines and eosinophil chemokines but enhanced TNFα-induced IL-8 production 2.01-fold compared with TNFα alone. <b>Conclusion:</b> Cigarette smoke may attenuate eosinophilic airway inflammation but promote neutrophilic airway inflammation in asthma.