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<p>Excessive neutrophil extracellular traps (NETs) formation is a significant contributor to acute lung injury (ALI), making its inhibition a novel therapeutic avenue to improve outcomes. In this study, we revealed that a novel pore-forming protein ninjurin-1 (NINJ1) was highly expressed in pro-inflammatory neutrophil subpopulations during ALI, using public single-cell RNA sequencing and hotspot analysis. Furthermore, we demonstrated that the NINJ1 oligomerization was essential for the NET release in neutrophils from both acute respiratory distress syndrome (ARDS) patients and ALI mice. Genetic ablation of <i>Ninj1</i> in neutrophils abolished NET release, thereby attenuating pulmonary dysfunction and reducing ALI-related lethality. Mechanistically, we found that K45 and N60 are critical for NINJ1 oligomerization and subsequent NET release. In summary, our findings reveal a novel pore-forming protein-mediated mechanism for NET release and highlight NINJ1 as a potential therapeutic target for the treatment of ALI/ARDS.</p><p></p>

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NINJ1 plays a vital role in the release of neutrophil extracellular traps during acute lung injury

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年6月25日

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  • Wen-Jing Zhong,
  • Yu-Biao Liu,
  • Xin-Yu Yang,
  • Meng-Rui Chen,
  • Nan-Shi-Yu Yang,
  • Chen-Yu Zhang,
  • Jian-Bing Xiong,
  • Wei-Feng Tang,
  • Cha-Xiang Guan,
  • Yan-Feng Zhang,
  • Jia-Xi Duan,
  • Yong Zhou

摘要

Excessive neutrophil extracellular traps (NETs) formation is a significant contributor to acute lung injury (ALI), making its inhibition a novel therapeutic avenue to improve outcomes. In this study, we revealed that a novel pore-forming protein ninjurin-1 (NINJ1) was highly expressed in pro-inflammatory neutrophil subpopulations during ALI, using public single-cell RNA sequencing and hotspot analysis. Furthermore, we demonstrated that the NINJ1 oligomerization was essential for the NET release in neutrophils from both acute respiratory distress syndrome (ARDS) patients and ALI mice. Genetic ablation of Ninj1 in neutrophils abolished NET release, thereby attenuating pulmonary dysfunction and reducing ALI-related lethality. Mechanistically, we found that K45 and N60 are critical for NINJ1 oligomerization and subsequent NET release. In summary, our findings reveal a novel pore-forming protein-mediated mechanism for NET release and highlight NINJ1 as a potential therapeutic target for the treatment of ALI/ARDS.