IL-17-Mediated Inflammation Promotes Cigarette Smoke-Induced Genomic Instability

Author:

Cao ChaoORCID,Tian Baoping,Geng Xinwei,Zhou Hongbin,Xu Zhiwei,Lai Tianwen,Wu Yanping,Bao Zhengqiang,Chen Zhihua,Li Wen,Shen Huahao,Ying Songmin

Abstract

(1) Background: Chronic inflammation has been regarded as a risk factor for the onset and progression of human cancer, but the critical molecular mechanisms underlying this pathological process have yet to be elucidated. (2) Methods: In this study, we investigated whether interleukin (IL)-17-mediated inflammation was involved in cigarette smoke-induced genomic instability. (3) Results: Higher levels of both IL-17 and the DNA damage response (DDR) were found in the lung tissues of smokers than in those of non-smokers. Similarly, elevated levels of IL-17 and the DDR were observed in mice after cigarette smoke exposure, and a positive correlation was observed between IL-17 expression and the DDR. In line with these observations, the DDR in the mouse lung was diminished in IL-17 KO when exposed to cigarette smoke. Besides this, the treatment of human bronchial epithelium cells with IL-17 led to increased levels of the DDR and chromosome breakage. (4) Conclusions: These results suggest that cigarette smoke induces genomic instability at least partially through IL-17-mediated inflammation, implying that IL-17 could play an important role in the development of lung cancer.

Funder

the Key Laboratory of Respiratory Disease of Zhejiang Province

the National Natural Science Foundation of China

Publisher

MDPI AG

Subject

General Medicine

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