The Role of Microglia in Modulating Neuroinflammation after Spinal Cord Injury

被引:75
|
作者
Brockie, Sydney [1 ]
Hong, James [1 ]
Fehlings, Michael G. [1 ,2 ,3 ]
机构
[1] Univ Hlth Network, Krembil Res Inst, Div Genet & Dev, Toronto, ON M5T 2S8, Canada
[2] Univ Toronto, Inst Med Sci, Toronto, ON M5S 1A8, Canada
[3] Univ Hlth Network, Toronto Western Hosp, Spinal Program, Toronto, ON M5T 2S8, Canada
关键词
spinal cord injury; microglia; neuroinflammation; FRACTALKINE-RECEPTOR; CEREBRAL-ISCHEMIA; NEUROPATHIC PAIN; INFLAMMATION; GABAPENTIN; MACROPHAGES; ACTIVATION; MECHANISMS; DISEASE; SYSTEM;
D O I
10.3390/ijms22189706
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
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页数:12
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