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Spinal cord injury (SCI) induces an immune response during which microglia, the resident immunocompetent cells of the central nervous system, become activated and migrate to the site of damage. Depending on their state of activation, microglia secrete neurotoxic or neurotrophic factors that influence the surrounding environment and have a detrimental or restorative effect following SCI, including causing or protecting bystander damage to nearby undamaged tissue.

Subsequent infiltration of macrophages contributes to the SCI outcome. We show here that suppressing microglia/macrophage activation using the tripeptide macrophage/microglia inhibitory factor (MIF/TKP) reduced secondary injury around the lesion epicenter in the murine dorsal hemisection model of SCI; it decreased the hypertrophic change of astrocytes and caused an increase in the number of axons present within the lesion epicenter. Moreover, timely inhibition of microglial/macrophage activation prevented demyelination and axonal dieback by modulating oligodendrocyte survival and oligodendrocyte precursor maturation. Microglia/macrophages located within or proximal to the lesion produced neurotoxic factors, such as tumor necrosis factor alpha (TNF-α). These results suggest that microglia/macrophages within the epicenter at early time points post injury are neurotoxic, contributing to demyelination and axonal degeneration and that MIF/TKP could be used in combination with other therapies to promote functional recovery.

Introduction Spinal cord injury (SCI) is a devastating trauma marked by the loss of sensory, motor and autonomic functions due to the degeneration of axons and glia. The initial insult to the central nervous system (CNS) causes necrosis of cells within the lesion epicenter, thereby inducing a cascade of biochemical and cellular events that lead to demyelination, degeneration of spared axons and inflammatory immune responses collectively referred to as secondary damage (; ). The necrosis triggers glial cell (e.g. Astrocytes, oligodendrocyte precursor cells, and microglia) activation and recruitment to the site of injury. Glial cell activation and the subsequent gliotic scar formation are thought to drive the ensuing secondary damage.

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In this setting, microglia, the resident CNS immune cells, release proinflammatory cytokines, reactive oxygen species and proteases that create bystander damage (; ). Chemokines produced by microglia, such as CCL2, CCL3, CXCL2/3 and CXCL10 are upregulated in minutes following injury (), recruit and activate peripheral polymorphonuclear leukocytes and monocytes which have been demonstrated to promote neurotoxicity (;;; ). On the other hand, the phagocytic properties of microglia and macrophages ensure myelin and tissue debris removal following the initial insult, which is necessary for proper remyelination of axons and neurite outgrowth (). In subsequent phases of the immune reaction, peripheral inflammatory cells such as neutrophils, macrophages and T-lymphocytes enter the lesioned area and release a plethora of cytokines that mediate detrimental effects through the generation of free radicals which promote apoptosis (). While there are some reports that suppression of the initial local inflammatory response following SCI reduces secondary injury around the lesion epicenter and improves functional outcome, other studies have provided evidence that inflammation supports regeneration via growth factors and cytokines released by activated microglia and macrophages.

Transplantation of in vitro activated microglia or macrophages within the injured spinal cord have been demonstrated to protect tissue, as well as promote axon regeneration and functional recovery via the release of trophic and anti-inflammatory factors (;;;; ). These restorative effects could be due to the release of trophic factors such as nerve growth factor (NGF), neurotrophin-3 (NT-3), interleukin-1 (IL-1), IL-10, and brain derived growth factor (BNDF), which influence axon regeneration.

Reports of heterogeneous subsets of microglia/macrophages render them to be either neurotoxic (M1) or neuroprotective (M2). Subsequent to injury, both M1 and M2 phenotypes are present, however shortly after the initial insult the M1 proinflammatory phenotype predominates, providing evidence that this neurotoxic phenotype may outweigh the neuroprotective phenotype (; ). Thus, therapeutic goals in the context of controlling microglial activation have remained unclear.

Macrophage/microglial inhibitory factor (MIF/TKP, tuftsin 1 fragment 1–3), a tripeptide (Thr-Lys-Pro, TKP) generated during the processing of immunoglobulin G, inhibits activation of cells of monocytic origin. For peripheral macrophages, MIF/TKP decreases cell migration, phagocytosis, chemotaxis and superoxide anion generation (). MIF/TKP also inhibits microglial function in the CNS. Administration of MIF/TKP during optic nerve trans-section has been reported to reduce axotomy-induced retinal ganglion cell degeneration () and to reduce demyelination and T-cell infiltration in the experimental allergic encephalomyelitis (EAE) model of multiple sclerosis, thereby abrogating disease symptoms and reducing lesion volume (); MIF/TKP also attenuates edema and decreases neuronal degeneration in intracerebral hemorrhage models (). Potential beneficial effects of MIF/TKP have not yet been examined in SCI. In this study, mice were treated with MIF/TKP and examined at various time points post SCI to assess consequences of inhibiting microglial/macrophage responses in a severe model of SCI. We demonstrate here that MIF/TKP administration alters the cellular and molecular environment to limit astrocyte hypertrophy, diminish oligodendrocyte cell death, and promote remyelination, leading to decreased secondary damage and axonal dieback.