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<p><i>Toxocara canis</i> is a globally distributed parasite that infects dogs and other canids, shedding eggs into the environment. Humans become accidental hosts by ingesting infective eggs, leading to syndromes such as visceral, ocular and neurotoxocariasis – the latter being poorly understood. Neurotoxocariasis has been proposed to be associated with epilepsy, cognitive impairment and schizophrenia, but its pathomechanism remains unclear. Here, we combine spatial transcriptomics, single-nucleus RNA sequencing, lipidomics and behavioural assays in a mouse model to characterise the host–parasite interface in the brain. <i>T. canis</i> larvae induce region-specific neural injury, vascular remodelling, and spatially confined immune responses, accompanied by parasite transcriptional programmes dominated by immunomodulatory factors and developmental regulators. Infected mice exhibit impairments in motor learning and memory, coinciding with transcriptional changes in neurons and glia. These findings provide mechanistic insight into neurotoxocariasis and demonstrate the utility of the mouse model as a platform to investigate helminth-induced neurological disorders.</p>

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Spatial transcriptomic atlas of murine neurotoxocariasis reveals region-specific host responses and dysfunction in the brain

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月17日

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  • Minyao Zou,
  • Sishi Liu,
  • Yi Chen,
  • Zhiwei Xiong,
  • Haiyan Wu,
  • Yi Yang,
  • Rongqiong Zhou,
  • Robin B. Gasser,
  • Guangxu Ma

摘要

Toxocara canis is a globally distributed parasite that infects dogs and other canids, shedding eggs into the environment. Humans become accidental hosts by ingesting infective eggs, leading to syndromes such as visceral, ocular and neurotoxocariasis – the latter being poorly understood. Neurotoxocariasis has been proposed to be associated with epilepsy, cognitive impairment and schizophrenia, but its pathomechanism remains unclear. Here, we combine spatial transcriptomics, single-nucleus RNA sequencing, lipidomics and behavioural assays in a mouse model to characterise the host–parasite interface in the brain. T. canis larvae induce region-specific neural injury, vascular remodelling, and spatially confined immune responses, accompanied by parasite transcriptional programmes dominated by immunomodulatory factors and developmental regulators. Infected mice exhibit impairments in motor learning and memory, coinciding with transcriptional changes in neurons and glia. These findings provide mechanistic insight into neurotoxocariasis and demonstrate the utility of the mouse model as a platform to investigate helminth-induced neurological disorders.