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Neuroimmune modulation for brain plasticity and repair

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Brain-immune system interactions have received growing attention in relation to a range of psychiatric (e.g. depression and schizophrenia) and neurodegenerative (e.g. Parkinson’s and Alzheimer’s disease) conditions. In particular, immune system messengers, called pro-inflammatory cytokines [e.g. interleukins ...

Brain-immune system interactions have received growing attention in relation to a range of psychiatric (e.g. depression and schizophrenia) and neurodegenerative (e.g. Parkinson’s and Alzheimer’s disease) conditions. In particular, immune system messengers, called pro-inflammatory cytokines [e.g. interleukins (ILs) and tumor necrosis factor-a (TNF-a)], foster a neuroinflammatory environment that can be damaging to neurons or disrupt neurotransmission. Immunocompetent microglial cells are primary brain sources of cytokines and are important for host defense, as well as being mediators of oxidative stress and pro-death pathways. Indeed, intereferon-g and TNF-a driven microglial activity has been implicated in neurodegenerative conditions, such as Parkinson’s and Alzheimer’s disease (PD and AD, respectively). At the same time, clinical and animal studies suggest an important role for IL-1b, TNF-a, as well as other inflammatory cytokines in stressor associated disorders, such as major depression.

Neuroinflammatory processes could promote neuronal pathology by negatively regulating endogenous protective factors. In this regard, an inflammatory milieu could impede anti-oxidant and anti-apoptotic defenses by interfering with normally protective trophic factor and neuroplastic responses. Such a link between neuroplasticity and immune factors is clearly evident when one considers the number of recent studies reporting that bacterial and viral agents, along with the pro-inflammatory cytokines, IL-1b, IL-6, TNF-a and IFN-a, all reduced hippocampal neurogenesis and affected synaptic plasticity and brain derived neurotrophic factor (BDNF) signaling. Importantly, BDNF reductions and impaired neuroplasticity have been implicated in numerous brain conditions, including PD, AD and depression. Conversely, antidepressant and neuroprotective treatments augment neurogenesis and BDNF expression.

Certain cytokines that have anti-inflammatory and trophic properties can promote neuroprotective actions and might even hold promise as adjunct anti-depressant agents. In particular, emerging evidence is beginning to reveal the beneficial neuronal effects of the hematopoietic cytokine, erythropoietin (EPO), as well as colony stimulating factors, such as granulocyte macrophage-colony stimulating factor (GM-CSF). Both these cytokines can protect neurons against the damaging effects of toxicants and cerebrovascular insults. Owing to their ability to induce BDNF and support neuroplastic processes, EPO and GM-CSF might also have positive neural actions with regards to cognitive and affective functioning. Similarly, anti-inflammatory cytokines, such as IL-10, can boost trophic support and impart neuroprotective outcomes.

This Frontiers special research topic involves a series of papers centered around the hypothesis that anti-inflammatory or immune-regulatory factors could provide a novel means of bolstering endogenous protective or reparative mechanisms (e.g. BDNF, anti-oxidant defenses) to combat neuropathology. Some papers will cover aspects of how immune regulatory treatments could have important neuroprotective consequences. Moreover, attention will be devoted to understanding how anti-inflammatory and/or immune modulatory factors can encourage neuroplasticity and potentially neuronal or functional recovery after damage has already occurred. Inflammatory routes to co-morbidity (such as depression) will also be covered, as will the possibility that neuroinflammatory biomarkers could be used to guide individualized treatments. Our aim is provide an integrative series of articles that could help steer the future search for novel strategies for harnessing the protective aspects of the neuroimmune system.


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