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在癌症患者中,G-CSF/NAMPT信号驱动中性粒细胞功能障碍并增强细菌感染易感性

Ekaterina Pylaeva^1,2, Lea Tollrian¹, Jana Riedesel¹

¹Department of Otorhinolaryngology, Head and Neck Surgery, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.

Nature communications

|December 12, 2025

概括

产生颗粒细胞殖民地刺激因子 (G-CSF) 的瘤会重编程中性粒细胞,损害它们对抗格兰氏阴性感染的能力. 准G-CSF/NAMPT通路可恢复中性粒细胞功能,并改善癌症中的细菌清除.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
微生物学微生物学

背景情况:

细菌感染是癌症治疗的一个重大挑战,导致治疗延迟和不良结果.
虽然免疫抑制和住院有所贡献,但它们并不能完全解释癌症患者感染风险的增加.
瘤衍生因素在损害宿主对病原体的防御机制方面发挥着作用.

研究的目的:

研究瘤在癌症患者中促进细菌感染的机制.
确定粒细胞殖民地刺激因子 (G-CSF) 和中性粒细胞重编程在细菌持久性中的作用.
评估向G-CSF/NAMPT途径用于癌症感染控制的治疗潜力.

主要方法:

对头部和部状细胞癌模型的分析.
对中性粒细胞原始体中的G-CSF/NAMPT信号轴的研究.
评估中性粒细胞的功能,包括细胞和中性粒细胞细胞外陷的形成.
在体内研究评估向G-CSF/NAMPT通路后的细菌清除.

主要成果:

瘤分泌高G-CSF水平诱导中性粒细胞重编程,促进了Gram-阴性病原体的持久性.
由瘤驱动的G-CSF/NAMPT激活会损害中性粒细胞的抗菌功能,并产生损伤组织的中性粒细胞子集.
这种重编程破坏了肺组织的完整性,促进了细菌的持久性.
准G-CSF/NAMPT通路逆转了中性粒细胞功能障碍,并在体内增强了细菌清除.

结论:

瘤诱导的,依赖于NAMPT的中性粒细胞重编程是癌症中抗菌防御受损的关键因素.
调节G-CSF/NAMPT信号通路为改善癌症患者感染控制和生存提供了潜在的治疗策略.

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