生物
细胞外
微生物学
炎症
细胞内
存水弯(水管)
趋化因子
作者
Weijie Chen,Jingjing Zhao,Di Mu,Zhuang Wang,Qin Liu,Yuanxing Zhang,Dahai Yang
出处
期刊:Journal of Immunology
[The American Association of Immunologists]
日期:2021-04-15
卷期号:206 (8): 1913-1922
被引量:26
标识
DOI:10.4049/jimmunol.2001335
摘要
Abstract The formation of neutrophil extracellular trap (NET) is a critical host defense when neutrophils migrate to infection sites. Pyroptosis is a newly identified programmed cell death, which is tightly regulated by inflammasome activation. However, the mechanism of pyroptotic signaling participating in NET production remains to be elucidated. In this study, the zebrafish larvae otic vesicle microinjection model was used to infect larvae with hemolysin-overexpressing Edwardsiella piscicida (EthA+), and a rapid migration of neutrophils to infection sites was observed. Intriguingly, EthA+ infection effectively induced significant neutrophil membrane rupture in vivo, which was dependent on caspase-B (caspy2) and gasdermin Eb (GSDMEb) but not caspase-A or gasdermin Ea. Specifically, the EthA+ E. piscicida infection induced pyroptosis along with NETosis in vitro, and depletion of either caspy2 or GSDMEb impaired NET formation in vivo. Consequently, inhibition of the caspy2–GSDMEb axis-gated NETosis impaired bacterial clearance in vivo. Altogether, these data provide evidence that teleost fish innate immune cells, including neutrophils, express features of pyroptosis that are critical for NETosis in teleost innate immunity.
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