S100B triggers neuroendocrine macrophage networks to drive airway regeneration in mice.

ABSTRACT: 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 S10

SUBMITTER: Sun B 

PROVIDER: S-EPMC12848069 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature