AI Article Synopsis
- IL-3 plays a significant role in lipid debris clearance by macrophages, which is crucial for recovery after spinal cord injuries (SCI), with its expression peaking at 14 days post-injury.
- Neutralizing IL-3 results in increased lipid accumulation and decreased neuronal survival, leading to greater motor deficits, while augmenting IL-3 promotes neuron preservation and enhances axon regeneration.
- These findings suggest that targeting the IL-3/IL-3Rα pathway could be a promising therapeutic approach for improving recovery after SCI.
Article Abstract
Background: Effective clearance of lipid-rich debris by macrophages is critical for neural repair and regeneration after spinal cord injury (SCI). Interleukin-3 (IL-3) has been implicated in programming microglia to cluster and clear pathological aggregates in neurodegenerative disease. Yet, the influence of IL-3 on lipid debris clearance post-SCI is not well characterized.
Methods: We established a mouse model of spinal cord compression injury to investigate the role of IL-3. Blockage of IL-3 was achieved through intrathecal delivery of an IL-3-neutralizing antibody, while IL-3 activation was augmented via in situ injection of recombinant IL-3 into the lesion site immediately post-SCI. Immunofluorescence staining was performed to determine IL-3 and IL-3Rα sources and distribution, lipid droplet accumulation, neuron preservation, and axon regeneration after SCI. The Basso Mouse Scale (BMS) and footprint analysis were employed to evaluate locomotor function recovery.
Results: We found that IL-3 expression was significantly upregulated post-SCI, peaking at 14 days post-injury (dpi) and persisting until 28 dpi. Notably, IL-3 was primarily secreted by astrocytes surrounding the lesion epicenter. Correspondingly, IL-3Rα was predominantly observed in macrophages within the injury core, also elevating at 14 dpi. Neutralization of IL-3 led to increased lipid droplet accumulation, along with markedly widespread of macrophages and decreased neuronal survival, resulting in severe motor deficits compared to controls. Conversely, in situ injection of IL-3 reduced lipid droplet accumulation in macrophages, preserved neurons, promoted axon regeneration, and ultimately contributed to the recovery of motor function after SCI.
Conclusion: Our findings shed light on the role of IL-3 in modulating macrophage phagocytic activity and suggest that the IL-3/IL-3Rα pathway may be a potential therapeutic target for enhancing neural repair and functional recovery after SCI.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11656101 | PMC |
| http://dx.doi.org/10.1111/cns.70181 | DOI Listing |
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