Page 261 - Read Online

Su Stroke, neuroinflammation, genetics

correlate with the degree of innate immune activity. For AVMs are abnormal vessels shunting blood directly
example, bone fracture induced systemic inflammation from arteries to veins [13] . AVM has abnormal vessel
exacerbates ischemic stroke injury in mice [3,4] and wall structure, which is likely to rupture. Rupture of
reduction of inflammation through activation of a-7 brain AVM can result in life-threatening intra-cranial
nicotinic acetylcholine receptor reduces ischemic brain hemorrhage and hemorrhagic stroke [13] . Alternatively,
[5]
injury . However, in recently years, many studies pulmonary AVMs in HHT type 1 patients are associated
showed that neuroinflammation appear to be double- with a higher incidence of paradoxical embolism in the
edged swords in the battle for neurological recovery. cerebral circulation causing ischemic brain injury than
For example, microglia/macrophage activation fosters general population.
brain recovery by clearing cell debris, which leads
to resolving local inflammation. Activated microglia/ ENG is required for the differentiation and sprouting
macrophage also produce a plethora of trophic factors of endothelial tubes, which are important processes
[6]
that promote tissue repair . Recent studies show of angiogenesis. ENG is also an important mediator
that blocking CCR2 macrophage impairs functional of endothelial-mesenchymal communication during
recovery of stroke victims . However, the kinetics of angiogenesis. Eng deficient mouse embryos show
[7]
macrophage/microglia polarization switch is different impaired recruitment of vascular smooth muscle cells
[12]
among different models, such as reperfusion vs. and pericytes to newly form vascular network. Zhu et al.
permanent occlusion [7,8] . Therefore, the contradictory discussed, in this issue, the roles of ENG in ischemic
functions of microglia/macrophage might reflect their stroke and indicated that ENG expression might be a
acquisition of distinct phenotypes in response to potential biomarker for vasospasm after subarachnoid
[6]
different microenvironmental cues . hemorrhage and cerebrovascular stenosis. Experimental
or therapeutic modulating of ENG expression could be
This issue includes a review and a mini review useful in generation of animal models for study disease
what discussed the role of inflammation in brain pathogenesis and for development of novel treatments
[9]
injury. Marcet et al. discussed the impacts of for multiple cerebrovascular diseases.
inflammation in ischemic stroke and traumatic brain
injury in their review. They indicated that although the In summary, we have tremendously expanded our
brain damage induced by the initial trauma is most working knowledge of how vascular remodeling in the
likely unsalvageable, the secondary immunologic brain occurs and identified many the key cellular and
deterioration of neural tissue gives many opportunities molecular events underlying this process in recently. In
for therapeutic strategists. This review highlighted this issue, we have assembled a collection of articles
the cell death mechanisms associated with injury or from renowned experts in the field of brain injury and
center nervous system (CNS) with special emphasis neuroinflammation, and attempted to lift some of the
on inflammation. They discussed the sources of veil on the pathophysiology of stroke.
inflammation, and introduced the role of the spleen in
the systemic response to inflammation after CNS injury. DECLARATIONS
In the mini-review, Liu et al. [10] overviewed the role of
microglia in neuroinflammatory after ischemic stroke. In
[11]
addition, a clinical study presented by Lu et al. in this Authors’ contributions
issue demonstrated a correlation of cerebral microbleed H. Su contributed solely to the paper.
and the level of inflammatory markers in blood.
Financial support and sponsorship
In addition to inflammatory, other such as genetic This study was supported by research grants from
variations influence stroke occurrence and recovery. A the National Institutes of Health (R01 NS027713, R01
review in this issue by Zhu et al. discussed the roles of HL122774 and R21 NS083788), Michael Ryan Zodda
[12]
endoglin gene in cerebral vascular diseases. Endoglin Foundation, to H.S.
(ENG) is a transforming growth factor beta associated
receptor and is required for both vasculogenesis and Conflicts of interest
angiogenesis. In human, ENG haploinsufficiency There are no conflicts of interest.
is associated with type 1 hereditary hemorrhagic
telangiectasia (HHT), also known as Osler-Rendu- Patient consent
Weber Syndrome, which is an autosomal dominant Not applicable.
disease. HHT patients have a higher prevalence of
telangiectases in mucocutaneous membrane and Ethics approval
arteriovenous malformation (AVM) in multiple organs. Not applicable.
Neuroimmunology and Neuroinflammation ¦ Volume 4 ¦ December 8, 2017 261