Enhanced Expression of PD-L1 on Microglia After Surgical Brain Injury Exerts Self-Protection from Inflammation and Promotes Neurological Repair

2019 ◽  
Vol 44 (11) ◽  
pp. 2470-2481 ◽  
Author(s):  
Qian Chen ◽  
Lixia Xu ◽  
Tianjiao Du ◽  
Yongxin Hou ◽  
Weijia Fan ◽  
...  
Keyword(s):  
Brain Injury ◽  
Enhanced Expression ◽  
Surgical Brain Injury ◽  
Self Protection

scholarly journals Preoperative mucosal tolerance to brain antigens and a neuroprotective immune response following surgical brain injury

2012 ◽  
Vol 116 (1) ◽  
pp. 246-253 ◽  
Author(s):  
Robert E. Ayer ◽  
Nazanin Jafarian ◽  
Wanqiu Chen ◽  
Richard L. Applegate ◽  
Austin R. T. Colohan ◽  
...  
Keyword(s):  
Brain Injury ◽  
Myelin Basic Protein ◽  
Cerebral Edema ◽  
Transforming Growth Factor ◽  
Basic Protein ◽  
Immunological Tolerance ◽  
Neurological Injury ◽  
Mucosal Tolerance ◽  
Surgical Brain Injury

Object Intracranial surgery causes cortical injury from incisions, hemorrhage, retraction, and electrocautery. The term “surgical brain injury” (SBI) has been developed to categorize this injury inherent to the procedure. Neuroinflammation plays a significant role in SBI. Traditional antiinflammatory therapies are often limited by their immunosuppressive side effects and poor CNS penetration. This study uses mucosal tolerance to develop an immune system that is tolerant to brain myelin basic protein (MBP) so that inflammation can be suppressed in a timely and site-specific manner following surgical disruption of the blood-brain barrier. Methods A standard SBI model using CD57 mice was used. Nasopharyngeal mucosa was exposed to vehicle, ovalbumin, or MBP to develop mucosal tolerance to these antigens. Immunological tolerance to MBP was confirmed in vivo through hypersensitivity testing. Neurological scores, cerebral edema, and interleukin (IL)–1β and transforming growth factor (TGF)–β1 cytokine levels were measured 48 hours postoperatively. Results Hypersensitivity testing confirmed the development of immune tolerance to MBP. Myelin basic protein–tolerant mice demonstrated reduced neurological injury, less cerebral edema, decreased levels of IL-1β, and increased levels of TGFβ1 following SBI. Conclusions Developing preoperative immunological tolerance to brain antigens through mucosal tolerance provides neuroprotection, reduces brain edema, and modulates neuroinflammation following SBI.

Correlation Between Subacute Sensorimotor Deficits and Brain Edema in Rats after Surgical Brain Injury

2016 ◽  
pp. 317-321
Author(s):  
Devin W. McBride ◽  
Yuechun Wang ◽  
Loic Adam ◽  
Guillaume Oudin ◽  
Jean-Sébastien Louis ◽  
...  
Keyword(s):  
Brain Injury ◽  
Brain Edema ◽  
Sensorimotor Deficits ◽  
Surgical Brain Injury

A Rat Model of Surgical Brain Injury

2019 ◽  
pp. 379-401
Author(s):  
Prativa Sherchan ◽  
Devin W. McBride ◽  
Lei Huang ◽  
Cesar Reis ◽  
Onat Akyol ◽  
...  
Keyword(s):  
Brain Injury ◽  
Rat Model ◽  
Surgical Brain Injury

scholarly journals Surgically-induced brain injury: where are we now?

2019 ◽  
Vol 5 (1) ◽  
Author(s):  
Zachary D. Travis ◽  
Prativa Sherchan ◽  
William K. Hayes ◽  
John H. Zhang
Keyword(s):  
Brain Injury ◽  
Brain Injuries ◽  
Neurosurgical Procedures ◽  
Cellular Mechanisms ◽  
The Past ◽  
Surgical Brain Injury ◽  
Neurosurgical Operation ◽  
Surgical Manipulations ◽  
Surgically Induced

AbstractNeurosurgical procedures cause inevitable brain damage from the multitude of surgical manipulations utilized. Incisions, retraction, thermal damage from electrocautery, and intraoperative hemorrhage cause immediate and long-term brain injuries that are directly linked to neurosurgical operations, and these types of injuries, collectively, have been termed surgical brain injury (SBI). For the past decade, a model developed to study the underlying brain pathologies resulting from SBI has provided insight on cellular mechanisms and potential therapeutic targets. This model, as seen in a rat, mouse, and rabbit, mimics a neurosurgical operation and causes commonly encountered post-operative complications such as brain edema, neuroinflammation, and hemorrhage. In this review, we elaborate on SBI and its clinical impact, the SBI animal models and their clinical relevance, the importance of applying therapeutics before neurosurgical procedures (i.e., preconditioning), and the new direction of applying venom-derived proteins to attenuate SBI.

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