Inflammasomes and gasdermins mount potent host defense pathways against invading microbial pathogens, however, dysregulation in these pathways can drive a variety of inflammatory disorders. Neutrophils, historically regarded as effector phagocytes that drive host defense via microbial killing, are now emerging as critical drivers of immunity in vivo. Here, we summarize, the latest advancement in inflammasome, gasdermin, and cell death signaling in neutrophils. We discuss the mechanisms by which neutrophils resist caspase-1-dependent pyroptosis, the lytic function of gasdermin D and E during NETosis and Yersinia infection, and the contribution of neutrophil inflammasomes to inflammatory disorders.

中文翻译：

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中性粒细胞中的炎性体和gasdermin信号传导

Inflammasomes 和 gasdermins 建立了有效的宿主防御途径来抵抗入侵的微生物病原体，然而，这些途径中的失调会导致各种炎症性疾病。中性粒细胞在历史上被认为是通过微生物杀伤来驱动宿主防御的效应吞噬细胞，现在正在成为体内免疫的关键驱动因素。在这里，我们总结了中性粒细胞炎症小体、gasdermin 和细胞死亡信号传导的最新进展。我们讨论了中性粒细胞抵抗 caspase-1 依赖性细胞焦亡的机制、gasdermin D 和 E 在 NETosis 和耶尔森菌感染期间的溶解功能，以及中性粒细胞炎症小体对炎症性疾病的贡献。