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<p>In mammals, a dysregulated immune response is detrimental to spinal cord repair. In zebrafish, which are capable of spinal cord regeneration, the immune response promotes regeneration. Neutrophils are the first immune cells to arrive at a spinal cord injury site, but their role in successful regeneration is not fully understood. Here we show that ablating neutrophils, including a subpopulation that expresses the cytokine <i>il4</i>, increases expression of <i>il1b</i> (coding for Il-1β) mainly in macrophages/microglia and delays anatomical and functional recovery after a spinal cord injury in larval zebrafish. Experimentally reducing Il-1β levels rescues axonal regeneration. Disruption of <i>il4</i> mimics the detrimental effect of neutrophil ablation for axonal regeneration and this is also rescued by reducing Il-1β levels. Moreover, after ablation of neutrophils, axonal regeneration and <i>il1b</i> expression levels are both rescued by over-expression of <i>il4</i>. Hence, after spinal cord injury, a pro-regenerative neutrophil subpopulation accelerates spinal cord regeneration in larval zebrafish by controlling expression of <i>il1b</i> mainly in macrophages/microglia. For this neutrophil action, <i>il4</i> expression is necessary and sufficient. </p>

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A reparative neutrophil subpopulation accelerates spinal cord regeneration in zebrafish by controlling macrophage inflammation via Il-4

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月26日

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  • Xiaobo Tian 田晓波,
  • Alberto Docampo-Seara,
  • Kim Heilemann,
  • Friederike Kessel,
  • Daniela Zöller,
  • Anja Bretschneider,
  • Thomas Becker,
  • Catherina G. Becker

摘要

In mammals, a dysregulated immune response is detrimental to spinal cord repair. In zebrafish, which are capable of spinal cord regeneration, the immune response promotes regeneration. Neutrophils are the first immune cells to arrive at a spinal cord injury site, but their role in successful regeneration is not fully understood. Here we show that ablating neutrophils, including a subpopulation that expresses the cytokine il4, increases expression of il1b (coding for Il-1β) mainly in macrophages/microglia and delays anatomical and functional recovery after a spinal cord injury in larval zebrafish. Experimentally reducing Il-1β levels rescues axonal regeneration. Disruption of il4 mimics the detrimental effect of neutrophil ablation for axonal regeneration and this is also rescued by reducing Il-1β levels. Moreover, after ablation of neutrophils, axonal regeneration and il1b expression levels are both rescued by over-expression of il4. Hence, after spinal cord injury, a pro-regenerative neutrophil subpopulation accelerates spinal cord regeneration in larval zebrafish by controlling expression of il1b mainly in macrophages/microglia. For this neutrophil action, il4 expression is necessary and sufficient.