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<p>Sepsis-induced acute lung injury (ALI) is a critical clinical condition characterized by severe inflammation and alveolar epithelial barrier disruption, with limited effective treatments. Our study investigates the role of Sbno2-expressing tissue-resident alveolar macrophages (TR-AMs) in promoting alveolar epithelial cell (AEC) regeneration and barrier function in sepsis-induced ALI. Utilizing single-cell RNA sequencing (scRNA-seq), we identified significant upregulation of Sbno2 in TR-AMs, which correlated with enhanced AEC proliferation and reduced apoptosis. Functional assays demonstrated that Sbno2-expressing TR-AMs substantially supported alveolar structure regeneration in both in vitro and in vivo models. Knockout of Sbno2 in TR-AMs impaired AEC proliferation and compromised lung barrier integrity. Therapeutic administration of recombinant Sbno2 (rSbno2) in a sepsis-induced ALI mouse model alleviated lung injury, promoted AEC proliferation, and restored barrier function, highlighting Sbno2 as a potential therapeutic target for ALI. These findings provide novel insights into the molecular mechanisms of lung repair in sepsis-induced ALI and suggest that enhancing Sbno2 expression in TR-AMs could be a promising strategy for improving outcomes in patients with ALI.</p>

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Sbno2-mediated tissue-resident alveolar macrophages: a novel therapeutic axis for sepsis-induced acute lung injury

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月5日

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  • Jingyu Dai,
  • Zhihai Wu,
  • Jiayi Zhong,
  • Xiaolong Wu,
  • Yibin Liu,
  • Qin Yang,
  • Li Li,
  • Shuyao Zhang,
  • Junyong Zhong

摘要

Sepsis-induced acute lung injury (ALI) is a critical clinical condition characterized by severe inflammation and alveolar epithelial barrier disruption, with limited effective treatments. Our study investigates the role of Sbno2-expressing tissue-resident alveolar macrophages (TR-AMs) in promoting alveolar epithelial cell (AEC) regeneration and barrier function in sepsis-induced ALI. Utilizing single-cell RNA sequencing (scRNA-seq), we identified significant upregulation of Sbno2 in TR-AMs, which correlated with enhanced AEC proliferation and reduced apoptosis. Functional assays demonstrated that Sbno2-expressing TR-AMs substantially supported alveolar structure regeneration in both in vitro and in vivo models. Knockout of Sbno2 in TR-AMs impaired AEC proliferation and compromised lung barrier integrity. Therapeutic administration of recombinant Sbno2 (rSbno2) in a sepsis-induced ALI mouse model alleviated lung injury, promoted AEC proliferation, and restored barrier function, highlighting Sbno2 as a potential therapeutic target for ALI. These findings provide novel insights into the molecular mechanisms of lung repair in sepsis-induced ALI and suggest that enhancing Sbno2 expression in TR-AMs could be a promising strategy for improving outcomes in patients with ALI.