Role of neuroinflammation in ischemic stroke

Once again describing a problem but offering NO solution. Now if we had a great stroke association we could update the stroke strategy to look for a solution. But we have jackshit for stroke leadership so nothing will get done.
http://nnjournal.net/article/view/1942

Rui Liu¹, Meng-Xian Pan¹, Jun-Chun Tang¹, Ya Zhang¹, Hua-Bao Liao¹, Yang Zhuang¹, Dan Zhao¹, Qi Wan^1,2

¹Department of Physiology, Collaborative Innovation Center for Brain Science, School of Basic Medical Sciences, School of Medicine, Wuhan University, Wuhan 430071, Hubei, China.

²Institute of Neuroregeneration and Neurorehabilitation, Qingdao University, Qingdao 266071, Shandong, China.

Correspondence Address: Dr. Qi Wan, Institute of Neuroregeneration and Neurorehabilitation, Qingdao University, 308 Ningxia Street, Qingdao 266071, Shandong, China. E-mail: qwanwh@hotmail.com

Dr. Qi Wan is a Professor in the Institute of Neuroregeneration and Neurorehabilitation at Qingdao University. He is also a Vice Dean for Research in the medical school. Before he joined to Qingdao University, he was a Professor at Wuhan University (2013-2017) and a tenured Associate Professor at University of Nevada at Reno (2008-2012) and a Senior Scientist in the Toronto Western Research Institute (2000-2008). His research is focused on understanding the cellular and molecular mechanisms underlying the roles of neurotransmitter receptors in synaptic plasticity and cerebral ischemic/reperfusion injury, and the role of endogenous neurogenesis in brain repair.
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Date of Submission           14-02-2017

Date of Acceptance           20-07-2017

Date of Web Publication    28-08-2017

DOI:10.20517/2347-8659.2017.09

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License (http://creativecommons.org/licenses/by-nc-sa/3.0/), which allows others to remix, tweak and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

How to cite this article:

Liu R, Pan MX, Tang JC, Zhang Y, Liao HB, Zhuang Y, Zhao D, Wan Q. Role of neuroinflammation in ischemic stroke. Neuroimmunol Neuroinflammation 2017;4:158-66.

Abstract

Ischemic stroke causes the depletion of energy and induce excitotoxicity and neuroinflammation in the brain that results from thrombotic blockage. Neuroinflammation occurs initially depending on activated resident microglia that has the same function as the macrophage. Activated microglia participates in the neuroinflammatory process by phagocytosing the injured brain cells and producing the pro- and anti-inflammatory mediators. In this review, the authors present an overview of the role of microglia in mediating neuroinflammation in ischemic stroke.

Key words: 
Microglia, 
ischemic stroke, 
neuroinflammation

Introduction

Stroke is an acute episode of focal dysfunction of the brain, retina or spinal cord lasting longer than 24 h, or for any duration if imaging (computed tomography or magnetic resonance imaging) or autopsy show focal infarction or hemorrhage relevant to the symptoms. Stroke is comprised of ischemic stroke (most common at approximately 85%) causing cerebral, retinal, and spinal infarction and hemorrhagic stroke (15%) that may result from intracerebral hemorrhage and subarachnoid hemorrhage [Figure 1]. Almost 90% of strokes are attributable to risk factors such as hypertension, regular physical inactivity, high apolipoprotein, insufficient diet quality, psychosocial factors, current smoking, cardiac causes, high alcohol consumption, and/or diabetes mellitus.[1]

Figure 1: Stroke is comprised of ischemic stroke (85%) and hemorrhagic stroke (15%) (intracerebral hemorrhage and subarachnoid hemorrhage)
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Ischemic stroke is caused by arterial embolism and in situ small vessel diseases. Embolism in brain results in oxygen and glucose deprivation, leading to brain damage and neurologic deficit. The cellular and molecular mechanisms underlying ischemic stroke-induced brain damage have been extensively investigated. Excitotoxicity, oxidative stress, and inflammation have been considered as major contributors to ischemic neuronal injury.[2] Cerebral ischemia induces large release of glutamate that causes over-activation of NMDA receptors and large inflow of Ca²⁺, leading to excitotoxicity-induced cell death.[3-7] The process of ischemia-reperfusion induces the production of superoxide and nitric oxide from damaged neurons and astrocytes and depletes glutathione, a primary antioxidant to protect against reactive oxygen species-mediated DNA damage.[8-10] Inflammation occurs after ischemia-reperfusion injury, which is caused by the dying cells and debris in the absence of microbes.[11,12]

There is an increasing evidence to showing complex role of the immune system in the pathophysiological changes that occur following ischemic stroke.[13] For example, brain injury activates neutrophils and macrophage/microglia,[14] as well as the lectin pathway of complement activation and the toll-like receptors (TLRs) that are the sensors in the innate immune system,[15,16] which leads to amplification of the inflammatory cascades. The immune system is closely involved in all the stages of ischemic stroke-induced brain damage and tissue repair by the parenchymal processes.[17,18] When activated, the adaptive immune system is intervened by lymphocyte populations that include T - B cells and regulatory T cells.[19] Additionally, stroke induces the deleterious antigen-specific autoreactive responses, but it also has beneficial effects.[20] The ischemic brain can act through the autonomic nervous system to have suppressive effect that can induce intercurrent infections and contribute to the morbidity and mortality after stroke.[21-23] Therefore, immune system-mediated inflammation is critically involved in determining the fate of the brain following ischemic stroke.[24-26] Understanding the mechanisms underlying role of neuroinflammation in ischemic stroke would provide important targets for the development of therapy in ischemic stroke.

The aim of this review is to offer an overview of the current knowledge about the immune system and the neuroinflammatory processes in ischemic stroke. We focus on how the neuroinflammatory processes are triggered by ischemic stroke, and how microglia cells play a role in neuroinflammation after ischemic stroke.

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