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Original Article
Neutrophil extracellular traps induced by cigarette smoke activate plasmacytoid dendritic cells
  1. Shi-Lin Qiu,
  2. Hui Zhang,
  3. Qi-ya Tang,
  4. Jing Bai,
  5. Zhi-Yi He,
  6. Jian-Quan Zhang,
  7. Mei-Hua Li,
  8. Jing-Min Deng,
  9. Guang-Nan Liu,
  10. Xiao-Ning Zhong
  1. Department of Respiratory Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, China
  1. Correspondence to Professor Xiao-Ning Zhong, Department of Respiratory Medicine, The FirstAffiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, China; xnzhong101{at}


Background Neutrophil extracellular traps (NETs) represent a distinct strategy by which neutrophils trap, confine and eliminate invading microorganisms. Emerging evidence suggests that NETs exert a deleterious effect to the host in the absence of microbial stimuli. However, the role of NETs in smoking-related lung diseases remains to be elucidated.

Objectives To evaluate the formation of NETs in the context of chronic inflammation induced by cigarette smoking and explore its potential role in an experimental mouse model of emphysema.

Methods The formation and degradation of NETs in cigarette smoke exposed mice was assessed with a fluorescence microscope. The potential influences of NETs on plasmacytoiddendritic cells were also investigated.

Results NETs were more prone to formation by polymorphonuclearneutrophils but defective in degradation in cigarette smoke exposed mice. Cigarette smoke extract (CSE) served as an important facilitator that triggered neutrophils to undergo NETosis in vitro. Furthermore, CSE-induced NETs were capable of driving plasmacytoiddendritic cell maturation and activation, thereby initiating a T-cell-mediated immune response.

Conclusions NETs may represent a critical connection between innate and adaptive immune responses under conditions of chronic inflammation induced by cigarette smoke exposure.

  • neutrophil extracellular traps
  • plasmacytoid dendritic cells
  • cigarette smoke

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  • Contributors Study design: XNZ and SLQ. Data acquisition and statistical analyses: SLQ, HZ, QYT, JB, ZYH, JQZ, MHL, MCD, JMD and GNL. Manuscript writing: SLQ and XNZ.

  • Funding This work was supported by grants from the National Natural Science Foundation of China (No. 81660007, No. 81260013 and No. 81260011).

  • Competing interests None declared.

  • Ethics approval Medical Ethical Committee of the First Affiliated Hospital of Guangxi Medical University.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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