Abstract
Interleukin-10 (IL-10) is an important anti-inflammatory cytokine expressed in response to brain injury, where it facilitates the resolution of inflammatory cascades, which if prolonged causes secondary brain damage. Here, we comprehensively review the current knowledge regarding the role of IL-10 in modulating outcomes following acute brain injury, including traumatic brain injury (TBI) and the various stroke subtypes. The vascular endothelium is closely tied to the pathophysiology of these neurological disorders and research has demonstrated clear vascular endothelial protective properties for IL-10. In vitro and in vivo models of ischemic stroke have convincingly directly and indirectly shown IL-10-mediated neuroprotection; although clinically, the role of IL-10 in predicting risk and outcomes is less clear. Comparatively, conclusive studies investigating the contribution of IL-10 in subarachnoid hemorrhage are lacking. Weak indirect evidence supporting the protective role of IL-10 in preclinical models of intracerebral hemorrhage exists; however, in the limited number of clinical studies, higher IL-10 levels seen post-ictus have been associated with worse outcomes. Similarly, preclinical TBI models have suggested a neuroprotective role for IL-10; although, controversy exists among the several clinical studies. In summary, while IL-10 is consistently elevated following acute brain injury, the effect of IL-10 appears to be pathology dependent, and preclinical and clinical studies often paradoxically yield opposite results. The pronounced and potent effects of IL-10 in the resolution of inflammation and inconsistency in the literature regarding the contribution of IL-10 in the setting of acute brain injury warrant further rigorously controlled and targeted investigation.
Highlights
Stroke and traumatic brain injury (TBI) are devastating acute neurological disorders that can result in high mortality rates or long-lasting disability
High IL-10 levels tend to predict worse outcomes after hemorrhagic brain injury, whereas the converse is true for brain ischemia, low IL-10 levels resulting from single nucleotide polymorphism (SNP) increase the risk for ischemic stroke (IS) and low levels after IS predict worse outcome
Preclinical models have shown that IL-10 administration after IS and TBI lend better outcomes, no work has been done in this area for subarachnoid hemorrhage (SAH) or intracerebral hemorrhage (ICH)
Summary
Stroke and traumatic brain injury (TBI) are devastating acute neurological disorders that can result in high mortality rates or long-lasting disability. Histone deacetylase plays a role in activating the expression of Foxp3 on Tregs, which secrete IL-10, and IL-10 was suggested as the main mediator of attenuated infarct volume and behavioral deficits, reduced levels of proinflammatory cytokines, and increased number of Tregs in the brain of MCAO mice with histone deacetylase inhibition [53].
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