IL‑17A and GDF15 are able to induce epithelial‑mesenchymal transition of lung epithelial cells in response to cigarette smoke
- Gang Jiang
- Chen‑Tao Liu
- Wei‑Dong Zhang
Affiliations: Department of Respiration, Hunan Provincial People's Hospital, Changsha, Hunan 410005, P.R. China, Department of Paediatrics, Xiang Ya Hospital, Central South University, Changsha, Hunan 410008, P.R. China
- Published online on: May 10, 2018 https://doi.org/10.3892/etm.2018.6145
Copyright: © Jiang
et al. This is an open access article distributed under the
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Smoking is one of the primary causes of chronic obstructive pulmonary disease (COPD). Sustained active epithelial‑mesenchymal transition (EMT) in COPD may explain the core pathophysiology of airway fibrosis and why lung cancer is so common among smokers. Interleukin (IL)‑17A and growth/differentiation factor (GDF)15 have been reported to be biomarkers of COPD; however, the role of IL‑17A and GDF15 in EMT remains unclear. The aim of the present study was to investigate the role of IL‑17A and GDF15 in the pathogenesis of COPD. It was demonstrated that IL‑17A and GDF15 are upregulated in patients with COPD, particularly those with a history of smoking. The results also revealed that IL‑17A and GDF15 expression was negatively correlated with the epithelial marker epithelial‑cadherin and positively correlated with the mesenchymal marker vimentin. Furthermore, treatment with cigarette smoke extract or IL‑17A induced GDF15 expression. Combined treatment with IL‑17A and GDF15 induced EMT in human small epithelial HSAEpiC cells in vitro. Collectively, the results of the present study suggest that IL‑17A and GDF15‑induced EMT serves an important role in the pathology of COPD.