Neutrophil extracellular traps induced by cigarette smoke activate plasmacytoid dendritic cells.

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

Qiu SL ，Zhang H ，Tang QY ，Bai J ，He ZY ，Zhang JQ ，Li MH ，Deng JM ，Liu GN ，Zhong XN ... -  《-》

Erythromycin suppresses neutrophil extracellular traps in smoking-related chronic pulmonary inflammation.

Zhang H ，Qiu SL ，Tang QY ，Zhou X ，Zhang JQ ，He ZY ，Bai J ，Li MH ，Deng JM ，Liang Y ，Zhong XN ... -  《Cell Death & Disease》

T lymphocyte priming by neutrophil extracellular traps links innate and adaptive immune responses.

Tillack K ，Breiden P ，Martin R ，Sospedra M ... -  《-》

Neutrophil extracellular traps induced by cigarette smoke contribute to airway inflammation in mice.

Neutrophil extracellular traps (NETs) were initially identified as an important antimicrobial barrier to capture and kill microorganisms. Emerging evidence suggests that NETs play a crucial role in chronic airway inflammation induced by cigarette smoke (CS). However, how NETs form and the mechanisms by which NETs function in CS-related airway diseases are still unclear. To explore NET formation and its potential role in CS-related airway diseases, we first established a CS-induced subacute airway inflammation model in mice and verified NET formation in the airways. Moreover, NETs degradation by aerosolized DNase I treatment significantly inhibited the airway inflammation induced by CS in mice. More importantly, by in vitro experiments, we found that cigarette smoke extract (CSE) induces NET formation in an NADPH oxidase-dependent manner, and that macrophages and human bronchial epithelial cells (HBEs) are important targets for the NETs-induced secretion of inflammatory cytokines. Therefore, NETs may represent a critical link among neutrophils, macrophages and HBEs under chronic inflammation conditions induced by CS.

Zou Y ，Chen X ，He B ，Xiao J ，Yu Q ，Xie B ，Yang S ，Dai L ，Dai Z ，Chen Q ... -  《-》

Innate immune processes are sufficient for driving cigarette smoke-induced inflammation in mice.

Botelho FM ，Gaschler GJ ，Kianpour S ，Zavitz CC ，Trimble NJ ，Nikota JK ，Bauer CM ，Stämpfli MR ... -  《-》