ArticleJournal of the peripheral nervous system : JPNS2020
Perisynaptic Schwann cells phagocytose nerve terminal debris in a mouse model of Guillain-Barré syndrome.
Article in Journal of the peripheral nervous system : JPNS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Vasculogenic tissue nanotransfection accelerates functional recovery after peripheral nerve injury.Science advances · 2026Article
- New Insights into Neuromuscular Junction Biology: Evidence from Human and Animal Research.International journal of molecular sciences · 2026Review
- Pathologic and Therapeutic Schwann Cells.Cells · 2025Review
- Absence of T-box transcription factor 21 limits neuromuscular junction recovery after nerve injury inFrontiers in cell and developmental biology · 2025Article
- Glial Regulation of Circuit Wiring, Firing, and Expiring in theCold Spring Harbor perspectives in biology · 2024Review
- Muscle Involvement in Amyotrophic Lateral Sclerosis: Understanding the Pathogenesis and Advancing Therapeutics.Biomolecules · 2023Review
- Response of terminal Schwann cells following volumetric muscle loss injury.Experimental neurology · 2023Article
- The endogenous calpain inhibitor calpastatin attenuates axon degeneration in murine Guillain-Barré syndrome.Journal of the peripheral nervous system : JPNS · 2023Article
- Neuron-Schwann cell interactions in peripheral nervous system homeostasis, disease, and preclinical treatment.Frontiers in cellular neuroscience · 2023Review
- Real time imaging of intra-axonal calcium flux in an explant mouse model of axonal Guillain-Barré syndrome.Experimental neurology · 2022Article
- Schwann cell nodal membrane disruption triggers bystander axonal degeneration in a Guillain-Barré syndrome mouse model.The Journal of clinical investigation · 2022Article
- Can lithium enhance the extent of axon regeneration and neurological recovery following peripheral nerve trauma?Neural regeneration research · 2022Article
- Heterogeneity and Potency of Peripheral Glial Cells in Embryonic Development and Adults.Frontiers in molecular neuroscience · 2022Review
- Axonal degeneration in Guillain-Barré syndrome: a reappraisal.Journal of neurology · 2021Review
- The Skeletal Muscle Emerges as a New Disease Target in Amyotrophic Lateral Sclerosis.Journal of personalized medicine · 2021Review
- Macrophage roles in peripheral nervous system injury and pathology: Allies in neuromuscular junction recovery.Molecular and cellular neurosciences · 2021Review
- Engulfed by Glia: Glial Pruning in Development, Function, and Injury across Species.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Review
- Terminal Schwann cells at the human neuromuscular junction.Brain communications · 2021Article
- Properties of Glial Cell at the Neuromuscular Junction Are Incompatible with Synaptic Repair in theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Perisynaptic Schwann cells phagocytose nerve terminal debris in a mouse model of Guillain-Barré syndrome.Journal of the peripheral nervous system : JPNS · 2020Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
In mouse models of acute motor axonal neuropathy, anti-ganglioside antibodies (AGAbs) bind to motor axons, notably the distal nerve, and activate the complement cascade. While complement activation is well studied in this model, the role of inflammatory cells is unknown. Herein we aimed to investigate the contribution of phagocytic cells including macrophages, neutrophils and perisynaptic Schwann cells (pSCs) to distal nerve pathology. To observe this, we first created a subacute injury model of sufficient duration to allow inflammatory cell recruitment. Mice were injected intraperitoneally with an anti-GD1b monoclonal antibody that binds strongly to mouse motor nerve axons. Subsequently, mice received normal human serum as a source of complement. Dosing was titrated to allow humane survival of mice over a period of 3 days, yet still induce the characteristic neurological impairment. Behaviour and pathology were assessed in vivo using whole-body plethysmography and post-sacrifice by immunofluorescence and flow cytometry. ex vivo nerve-muscle preparations were used to investigate the acute phagocytic role of pSCs following distal nerve injury. Following complement activation at distal intramuscular nerve sites in the diaphragm macrophage localisation or numbers are not altered, nor do they shift to a pro- or anti-inflammatory phenotype. Similarly, neutrophils are not significantly recruited. Instead, ex vivo nerve-muscle preparations exposed to AGAb plus complement reveal that pSCs rapidly become phagocytic and engulf axonal debris. These data suggest that pSCs, rather than inflammatory cells, are the major cellular vehicle for axonal debris clearance following distal nerve injury, in contrast to larger nerve bundles where macrophage-mediated clearance predominates.
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