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<p>Spinal cord injuries (SCIs) often result in permanent disabilities in humans. One major reason for the lack of recovery is the inability of adult mammalian descending neurons to regenerate their axons after injury. In contrast, several fish species, such as the sea lamprey, exhibit spontaneous axon regeneration and successful functional recovery following a complete SCI. Recent studies have shown that a SCI in rodents and humans induces gut microbiome dysbiosis, which can impair recovery. Therefore, our goal was to examine how the microbiome changes after SCI in a regenerating animal model (the larval sea lamprey) and whether these changes influence the spontaneous regeneration of descending neuropeptidergic (cholecystokinergic) axons. Our data show that a complete SCI triggers an initial shift (5 weeks post-injury) in gut microbial communities in larval lampreys, characterized by an expansion of <i>Legionellaceae</i> family members. However, a treatment with broad-spectrum antibiotic gentamicin during the first 5 weeks post-injury, which profoundly altered the gut microbiome (eliminating <i>Legionellaceae</i> and promoting <i>Bradyrhizobiaceae</i> expansion), did not affect the spontaneous regeneration of descending cholecystokinergic axons at 10 weeks post-injury. This finding indicates that broad gentamicin-induced disruption of the gut microbiota does not detectably impair spontaneous regeneration of descending cholecystokinergic axons in larval lampreys.</p>

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Spontaneous axon regeneration is preserved despite gut microbiota disruption after spinal cord injury in larval lampreys

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月2日

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  • Laura González-Llera,
  • Gabriel N. Santos-Durán,
  • Ana Vences,
  • Noemí Buján,
  • Miguel Balado,
  • Antón Barreiro-Iglesias

摘要

Spinal cord injuries (SCIs) often result in permanent disabilities in humans. One major reason for the lack of recovery is the inability of adult mammalian descending neurons to regenerate their axons after injury. In contrast, several fish species, such as the sea lamprey, exhibit spontaneous axon regeneration and successful functional recovery following a complete SCI. Recent studies have shown that a SCI in rodents and humans induces gut microbiome dysbiosis, which can impair recovery. Therefore, our goal was to examine how the microbiome changes after SCI in a regenerating animal model (the larval sea lamprey) and whether these changes influence the spontaneous regeneration of descending neuropeptidergic (cholecystokinergic) axons. Our data show that a complete SCI triggers an initial shift (5 weeks post-injury) in gut microbial communities in larval lampreys, characterized by an expansion of Legionellaceae family members. However, a treatment with broad-spectrum antibiotic gentamicin during the first 5 weeks post-injury, which profoundly altered the gut microbiome (eliminating Legionellaceae and promoting Bradyrhizobiaceae expansion), did not affect the spontaneous regeneration of descending cholecystokinergic axons at 10 weeks post-injury. This finding indicates that broad gentamicin-induced disruption of the gut microbiota does not detectably impair spontaneous regeneration of descending cholecystokinergic axons in larval lampreys.