http://nnjournal.net/article/view/1942
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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