Neuroimmune Response in Ischemic Preconditioning

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...

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Bibliographic Details
Published in:Neurotherapeutics 2016-10, Vol.13 (4), p.748-761
Main Authors: McDonough, Ashley, Weinstein, Jonathan R.
Format: Article
Language:English
Subjects:
Animals
Biomedical and Life Sciences
Biomedicine
Brain Ischemia - complications
Brain Ischemia - immunology
Brain Ischemia - pathology
Cytokines - metabolism
Encephalitis - etiology
Humans
Ischemic Preconditioning
Microglia
Neurobiology
Neurology
Neurosciences
Neurosurgery
Review
Stroke - prevention & control
Toll-Like Receptors - metabolism
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Summary: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 pro- and 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.
ISSN:1933-7213
1878-7479
DOI:10.1007/s13311-016-0465-z