Neutrophil death can transpire via diverse pathways and is regulated by interactions with commensal and pathogenic microorganisms, environmental exposures, and cell age. At steady state, neutrophil turnover and replenishment are continually maintained via a delicate balance between host-mediated responses and microbial forces. Disruptions in this equilibrium directly impact neutrophil numbers in circulation, cell trafficking, antimicrobial defenses, and host well-being. How neutrophils meet their end is physiologically important and can result in different immunologic consequences. Whereas nonlytic forms of neutrophil death typically elicit anti-inflammatory responses and promote healing, pathways ending with cell membrane rupture may incite deleterious proinflammatory responses, which can exacerbate local tissue injury, lead to chronic inflammation, or precipitate autoimmunity. This review seeks to provide a contemporary analysis of mechanisms of neutrophil death.

中文翻译：

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中性粒细胞如何达到目的。

中性粒细胞的死亡可以通过多种途径发生，并受与共生和病原微生物的相互作用，环境暴露和细胞年龄的调节。在稳定状态下，通过宿主介导的反应和微生物力之间的微妙平衡，持续保持中性粒细胞的更新和补充。这种平衡的破坏直接影响循环中的中性粒细胞数量，细胞运输，抗微生物防御和宿主健康。中性粒细胞如何达到其末端在生理上很重要，并可能导致不同的免疫学后果。非溶性中性粒细胞死亡通常会引发抗炎反应并促进愈合，而以细胞膜破裂为终点的途径可能会引起有害的促炎反应，从而加剧局部组织损伤，导致慢性炎症或促进自身免疫。这篇综述旨在提供中性粒细胞死亡机制的当代分析。