This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research
IL-17-mediated inflammation promotes cigarette smoke-induced genomic instability
Songmin Ying
Zhejiang University
Corresponding Author
License:
This work is licensed under a CC BY 4.0 License. Read Full License
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 has yet to be elucidated.
Methods
In this study, we investigated whether interleukin (IL)-17-mediated inflammation was involved in cigarette smoke-induced genomic instability.
Results
Higher levels of both IL-17 and the DNA damage response (DDR) were found in the lung tissue of smokers than that 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, the treatment of human bronchial epithelium cells with IL-17 led to increased levels of the DDR and chromosome breakage.
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.
Keywords
IL-17, Inflammation, Cigarette smoke, DNA damage response
Figure 1
Figure 2
Figure 3
Figure 4
This is a list of supplementary files associated with this preprint. Click to download.
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 23 Feb, 2021
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cancer Biology
Learn more about our company.
This is a preprint. It has not completed peer review.
Research
IL-17-mediated inflammation promotes cigarette smoke-induced genomic instability
Songmin Ying
Zhejiang University
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 23 Feb, 2021
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cancer Biology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
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 has yet to be elucidated.
Methods
In this study, we investigated whether interleukin (IL)-17-mediated inflammation was involved in cigarette smoke-induced genomic instability.
Results
Higher levels of both IL-17 and the DNA damage response (DDR) were found in the lung tissue of smokers than that 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, the treatment of human bronchial epithelium cells with IL-17 led to increased levels of the DDR and chromosome breakage.
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.
Figure 1
Figure 2
Figure 3
Figure 4