Abstract
The pathobiology of traumatic and nontraumatic spinal cord injury (SCI), including degenerative myelopathy, is influenced by neuroinflammation. The neuroinflammatory response is initiated by a multitude of injury signals emanating from necrotic and apoptotic cells at the lesion site, recruiting local and infiltrating immune cells that modulate inflammatory cascades to aid in the protection of the lesion site and encourage regenerative processes. While peripheral immune cells are involved, microglia, the resident immune cells of the central nervous system (CNS), are known to play a central role in modulating this response. Microglia are armed with numerous cell surface receptors that interact with neurons, astrocytes, infiltrating monocytes, and endothelial cells to facilitate a dynamic, multi-faceted injury response. While their origin and essential nature are understood, their mechanisms of action and spatial and temporal profiles warrant extensive additional research. In this review, we describe the role of microglia and the cellular network in SCI, discuss tools for their investigation, outline their spatiotemporal profile, and propose translationally-relevant therapeutic targets to modulate neuroinflammation in the setting of SCI.
Highlights
Injury to the spinal cord can be caused by acute trauma or progressive compression from myelopathic mechanisms [1,2]
The lesion site becomes littered with necrotic cells and debris, as well as blood and cerebrospinal fluid caused by disruption of the blood spinal cord barrier
Surgical decompression is the most effective treatment for both forms of spinal cord injury (SCI) to date [1,4], but recovery is limited by the inflammatory response that results from the restoration of blood flow across damaged tissue, causing extensive secondary damage that exacerbates the initial injury [5]
Summary
Injury to the spinal cord can be caused by acute trauma or progressive compression from myelopathic mechanisms [1,2]. Surgical decompression is the most effective treatment for both forms of SCI to date [1,4], but recovery is limited by the inflammatory response that results from the restoration of blood flow across damaged tissue, causing extensive secondary damage that exacerbates the initial injury [5]. Both phases of inflammation are characterized by well-described neuroinflammatory responses whereby resident microglia and neutrophils respond first, followed by infiltrating monocytes. Nonspecific markers of microglia and macrophages [18]
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