The Impact of Nuclear Factor Kappa B on the Response of Microglia in Spinal Cord Injuries

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Spinal cord injury (SCI) results in both primary and secondary damage, each contributing to the overall injury and its consequences. Following SCI, microglia, the resident immune cells of the central nervous system (CNS), undergo a series of complex responses that contribute to the pathophysiology of the injury. In the context of SCI, nuclear factor kappa B (NF-kB) emerged as a critical mediator in the regulation of inflammatory responses following SCI. The aim of this review is to provide a comprehensive understanding of the involvement of NF-kB in the response of microglia following SCI. The PUBMED database was searched using the following keywords: NF-kB AND microglia AND spinal cord injury. Clinical and experimental studies evaluating the role of NF-kB in the response of microglia following SCI were included. Systematic reviews, case reports, research protocols, conference articles, and studies in languages other than English were excluded. The final analysis included 52 studies. NF-kB signaling exerts profound effects on the microglial response following SCI, influencing the inflammatory milieu, tissue damage, and potential for repair and recovery. Deactivation of the NF-kB signaling pathway suppresses the production of proinflammatory mediators in microglia, after SCI. Moreover, NF-kB suppression has neuroprotective effects, as it mitigates neuronal apoptosis and facilitates the M2 microglial phenotype, alleviating tissue damage after SCI. Moreover, several microRNAs play a crucial role in regulating gene expression post-transcriptionally and have emerged as key regulators in microglia activation after SCI. Overall, the role of NF-kB in the response of microglia to SCI is complex and context-dependent. While NF-kB activation is involved in initiating and propagating the inflammatory response following SCI, it also plays a role in tissue repair and regeneration. Thus, modulating NF-kB signaling in microglia represents a potential therapeutic target for attenuating inflammation and promoting neuroprotection and tissue repair in SCI.

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