Macrophage activation and its role in repair and pathology after spinal cord injury.

By J. Gensel, Bei Zhang. Brain Research, 2015

695 citations recorded by the source corpus.

The injured spinal cord does not heal properly. In contrast, tissue repair and functional recovery occur after skin or muscle injuries. The reason for this dichotomy in wound repair is unclear but inflammation, and specifically macrophage activation, likely plays a key role. Macrophages have the ability to promote the repair of injured tissue by regulating transitions through different phase of the healing response. In the current review we compare and contrast the healing and inflammatory responses between spinal cord injuries and tissues that undergo complete wound resolution. Through this comparison, we identify key macrophage phenotypes that are inaptly triggered or absent after spinal cord injury and discuss spinal cord stimuli that contribute to this maladaptive response. Sequential activation of classic, pro-inflammatory, M1 macrophages and alternatively activated, M2a, M2b, and M2c macrophages occurs during normal healing and facilitates transitions through the inflammatory, proliferative, and remodeling phases of repair. In contrast, in the injured spinal cord, pro-inflammatory macrophages potentiate a prolonged inflammatory phase and remodeling is not properly initiated. The desynchronized macrophage activation after spinal cord injury is reminiscent of the inflammation present in chronic, non-healing wounds. By refining the role macrophages play in spinal cord injury repair we bring to light important areas for future neuroinflammation and neurotrauma research. This article is part of a Special Issue entitled SI: Spinal cord injury.

Subfields: Endocrinology, Diabetes and Metabolism, Pathology and Forensic Medicine, Rehabilitation

View Paper: https://www.semanticscholar.org/paper/ae3409d20220e7432649296978cfe87ed8b94b93

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In Pathology and Forensic Medicine

Citations in the corpus

Microglia in the TBI Brain: The Good, The Bad, And The Dysregulated (2015, background): “…was similar to the damage response ofwound-healingmacrophages outside the CNS, such that proinflammatory and proteolytic macrophages accumulate rapidly after injury, followed by macrophages that promote wound-healing and antiinflammatory responses (Deonarine et al., 2007; Gensel and Zhang, 2015).”