Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, China
Copyright 2016, American College of Chest Physicians. All Rights Reserved.
SESSION TITLE: Tobacco Cessation and Prevention
SESSION TYPE: Original Investigation Poster
PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM
PURPOSE: In this study, we aim to investigate whether cigarette smoke was able to induce DNA damage response (DDR) and genomic instability in multiple tissues as well as whether interleukin (IL)-17 involved in cigarette smoke-induced genomic instability.
METHODS: C57BL/6 mice and IL-17 knockout mice were exposed 5 d/week for 12 weeks or 24 weeks. DDR of multiple organs and BALF cells was studied. DDR, chromosome breakage, and cell cycle arrest of airway epithelial cells after IL-17 treatment was further studied.
RESULTS: The current study showed that cigarette smoke-exposure induced DDR in the lung and bladder. In addition, cigarette smoke-exposure promoted IL-17 expression and airway inflammation. A positive correlation was observed between IL-17 expression and DDR. IL-17 treatment induced DDR and chromosome breakage of airway epithelial cells. After treated with IL-17, the majority of γH2AX foci were observed in cells expressing cyclin A, a marker of cells in S/G2 phase. It is surprising that DDR in the lung of mice was diminished in IL-17 knockout mice when exposed to cigarette smoke.
CONCLUSIONS: These results suggest that cigarette smoke-induced genomic instability in the lung and bladder. IL-17-mediated inflammation promotes cigarette smoke-induced genomic instability.
CLINICAL IMPLICATIONS: These findings imply that IL-17 antibody may be promising drugs for the treatment against cigarette smoke-related diseases.
DISCLOSURE: The following authors have nothing to disclose: Chao Cao, Hongbin Zhou, Bao-ping Tian, Zhihua Chen, Wen Li, Songmin Ying, Huahao Shen
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