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<p>The mammalian airway epithelium contains specialized cells that detect and respond to environmental injury, yet the mechanisms that coordinate epithelial repair remain poorly defined. Pulmonary neuroendocrine cells act as neurosensory sentinels within this epithelium and can reprogram to support regeneration. Here we show that the calcium-binding protein S100B is essential for maintaining the stem cell-like properties of pulmonary neuroendocrine cells during airway repair. Following epithelial injury, S100B expression is induced in these cells and released to engage macrophages that express the enzyme arginase-1, which in turn promotes the expansion of pulmonary neuroendocrine cells and their transition into regenerative intermediate cells. Modulating S100B activity, either by blocking S100B with pentamidine or by enhancing signaling driven by the protein kinase p110-alpha in airway epithelial cells, alters the reparative capacity of pulmonary neuroendocrine cells. These findings identify an S100B-arginase-1 signaling axis that governs macrophage-epithelial communication and highlight S100B as a potential therapeutic target for lung repair.</p>

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S100B triggers neuroendocrine macrophage networks to drive airway regeneration in mice

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年12月17日

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  • Bing Sun,
  • Haiting Dai,
  • Tiemei Zhao,
  • Yun Guo,
  • Yujia Liu,
  • Wenya Li,
  • Mingli Zhu,
  • Yilina Bai,
  • Hanyuhui Yang,
  • Yiming Xing

摘要

The mammalian airway epithelium contains specialized cells that detect and respond to environmental injury, yet the mechanisms that coordinate epithelial repair remain poorly defined. Pulmonary neuroendocrine cells act as neurosensory sentinels within this epithelium and can reprogram to support regeneration. Here we show that the calcium-binding protein S100B is essential for maintaining the stem cell-like properties of pulmonary neuroendocrine cells during airway repair. Following epithelial injury, S100B expression is induced in these cells and released to engage macrophages that express the enzyme arginase-1, which in turn promotes the expansion of pulmonary neuroendocrine cells and their transition into regenerative intermediate cells. Modulating S100B activity, either by blocking S100B with pentamidine or by enhancing signaling driven by the protein kinase p110-alpha in airway epithelial cells, alters the reparative capacity of pulmonary neuroendocrine cells. These findings identify an S100B-arginase-1 signaling axis that governs macrophage-epithelial communication and highlight S100B as a potential therapeutic target for lung repair.