Functional polarization of neuroglia: Implications in neuroinflammation and neurological disorders

Jha, Mithilesh Kumar; Lee, Won‐Ha; Suk, Kyoungho

doi:10.1016/j.bcp.2015.11.003

“…The pioneering papers in the RIPC field suggest that neuroprotection is induced rapidly [30,31,37]; however, the duration of protection has not been determined [37,38]. Molecular determinants behind the phenomenon of RIPC have not been fully elucidated, but there is some evidence of overlap with molecular mediators of ischemic and LPS preconditioning, including hypoxiainducible factor (HIF)-1α [39], and inflammatory factors [40][41][42][43]. Remote limb ischemia may induce global expression of these molecular mediators of preconditioning that confers protection to multiple organ systems, including the brain.…”

Section: Hif-1mentioning

confidence: 99%

“…Remote limb ischemia may induce global expression of these molecular mediators of preconditioning that confers protection to multiple organ systems, including the brain. Some studies of remote limb ischemia have demonstrated reduced inflammation in multiple organs after preconditioning [42,43], which suggests that ischemic protection via modulation of immune responses may extend to the entire body and not just be localized to a single organ or region of the body. Recent clinical trials on the efficacy of RIPC found no significant difference in composite endpoints in patients treated with RIPC and those which received sham RIPC treatment prior to cardiac surgery [32,33].…”

Section: Hif-1mentioning

confidence: 99%

Neuroimmune Response in Ischemic Preconditioning

McDonough

¹

,

Weinstein

²

2016

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Ischemic preconditioning (IPC) is a robust neuroprotective phenomenon in which a brief period of cerebral ischemia confers transient tolerance to subsequent ischemic challenge. Research on IPC has implicated cellular, molecular, and systemic elements of the immune response in this phenomenon. Potent molecular mediators of IPC include innate immune signaling pathways such as Toll-like receptors and type 1 interferons. Brain ischemia results in release of proand anti-inflammatory cytokines and chemokines that orchestrate the neuroinflammtory response, resolution of inflammation, and transition to neurological recovery and regeneration. Cellular mediators of IPC include microglia, the resident central nervous system immune cells, astrocytes, and neurons. All of these cell types engage in cross-talk with each other using a multitude of signaling pathways that modulate activation/ suppression of each of the other cell types in response to ischemia. As the postischemic neuroimmune response evolves over time there is a shift in function toward provision of trophic support and neuroprotection. Peripheral immune cells infiltrate the central nervous system en masse after stroke and are largely detrimental, with a few subtypes having beneficial, protective effects, though the role of these immune cells in IPC is largely unknown. The role of neural progenitor cells in IPC-mediated neuroprotection is another active area of investigation as is the role of microglial proliferation in this setting. A mechanistic understanding of these molecular and cellular mediators of IPC may not only facilitate more effective direct application of IPC to specific clinical scenarios, but also, more broadly, reveal novel targets for therapeutic intervention in stroke.

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“…However, the full extent and mechanisms of IFN signaling in IPCmediated protection remain to be explored. The cellular source of IFN-β in the postischemic brain is unknown, but there are several possible sources such as peripheral macrophages [53,54] and astrocytes [55][56][57][58]. Published studies also suggest neurons [59] are capable of releasing IFN-β under specific conditions.…”

Section: Molecular Mediators Of Preconditioningmentioning

confidence: 99%

“…Microglia contribute to the maintenance of brain homeostasis, suggesting a critical role for microglia in the normal physiology of the CNS [56], and pathway analysis of baseline microglial gene expression (from naïve wild-type mouse brain) revealed that the functions most associated with microglia were related to nervous system development [82].…”

Section: Microgliamentioning

confidence: 99%

Correction to: Neuroimmune Response in Ischemic Preconditioning

McDonough

¹

,

Weinstein

²

2018

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Ischemic preconditioning (IPC) is a robust neuroprotective phenomenon in which a brief period of cerebral ischemia confers transient tolerance to subsequent ischemic challenge. Research on IPC has implicated cellular, molecular, and systemic elements of the immune response in this phenomenon. Potent molecular mediators of IPC include innate immune signaling pathways such as Tolllike receptors and type 1 interferons. Brain ischemia results in release of pro-and anti-inflammatory cytokines and chemokines that orchestrate the neuroinflammatory response, resolution of inflammation, and transition to neurological recovery and regeneration. Cellular mediators of IPC include microglia, the resident central nervous system immune cells, astrocytes, and neurons. All of these cell types engage in cross-talk with each other using a multitude of signaling pathways that modulate activation/ suppression of each of the other cell types in response to ischemia. As the postischemic neuroimmune response evolves over time there is a shift in function toward provision of trophic support and neuroprotection. Peripheral immune cells infiltrate the central nervous system en masse after stroke and are largely detrimental, with a few subtypes having beneficial, protective effects, though the role of these immune cells in IPC is largely unknown. The role of neural progenitor cells in IPC-mediated neuroprotection is another active area of investigation as is the role of microglial proliferation in this setting. A mechanistic understanding of these molecular and cellular mediators of IPC may not only facilitate more effective direct application of IPC to specific clinical scenarios, but also, more broadly, reveal novel targets for therapeutic intervention in stroke. Keywords PreconditioningIschemic preconditioning (IPC) is an experimental phenomenon in which a brief period of ischemia confers robust neuroprotection against subsequent ischemic events [1-3]. It is important to note that preconditioning does not reduce the incidence of stroke, but rather ameliorates the pathophysiologic response to cerebral ischemia and results in a smaller infarct volume and improved poststroke recovery [4][5][6]. Clinical studies suggest that patients with stroke who suffered a recent prior transient ischemic attack have better outcomes than those who did not, implying that a human correlate to experimental IPC exists [7,8]. Elucidating the mechanisms of IPC is considered a critical challenge in stroke research [9,10]. Recent literature has implicated innate immune pathways, including Toll-like receptors (TLRs) [11,12] and type 1 interferon (IFN) signaling [5,11,13] in IPC-mediated protection.Due to a technical error in the production process, the earlier version of this article contained numerous errors in the reference numbering. We are reprinting the entire article in the correction for readabilityThe online version of the original article can be found at https://doi

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“…Els tipus fonamentals de glies en el SNC són els astròcits, l'oligodendròglia i la micròglia. D'ells, els astròcits i la micròglia són probablement les classes de glia més directament relacionades amb la resposta a les lesions neurodegeneratives i les que s'activen en la resposta neuroinflamatòria (Jha, 2015), i per tant són les que discutirem a continuació.…”

Section: El Sistema Nerviós Quelcom Més Que Neuronesunclassified

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varios¹

2016

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Functional polarization of neuroglia: Implications in neuroinflammation and neurological disorders

Cited by 230 publications

References 233 publications

Neuroimmune Response in Ischemic Preconditioning

Neuroimmune Response in Ischemic Preconditioning

Correction to: Neuroimmune Response in Ischemic Preconditioning

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