scholarly journals The Role of the Choroid Plexus in Neutrophil Invasion after Traumatic Brain Injury

2009 ◽  
Vol 29 (9) ◽  
pp. 1503-1516 ◽  
Author(s):  
Joanna Szmydynger-Chodobska ◽  
Nathalie Strazielle ◽  
Brian J Zink ◽  
Jean-François Ghersi-Egea ◽  
Adam Chodobski
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Choroid Plexus ◽  
Neutrophil Migration ◽  
Inflammatory Cells ◽  
Brain Parenchyma ◽  
Electron Microscopic ◽  
Epithelial Barriers

Traumatic brain injury (TBI) frequently results in neuroinflammation, which includes the invasion of neutrophils. After TBI, neutrophils infiltrate the choroid plexus (CP), a site of the blood—cerebrospinal fluid (CSF) barrier (BCSFB), and accumulate in the CSF space near the injury, from where these inflammatory cells may migrate to brain parenchyma. We have hypothesized that the CP functions as an entry point for neutrophils to invade the injured brain. Using the controlled cortical impact model of TBI in rats and an in vitro model of the BCSFB, we show that the CP produces CXC chemokines, such as cytokine-induced neutrophil chemoattractant (CINC)-1 or CXCL1, CINC-2α or CXCL3, and CINC-3 or CXCL2. These chemokines are secreted both apically and basolaterally from the choroidal epithelium, a prerequisite for neutrophil migration across epithelial barriers. Consistent with these findings, we also provide electron microscopic evidence that neutrophils infiltrate the choroidal stroma and subsequently reach the intercellular space between choroidal epithelial cells. This is the first detailed analysis of the BCSFB function related to neutrophil trafficking. Our observations support the role of this barrier in posttraumatic neutrophil invasion.

Role of synucleins in traumatic brain injury — An experimental in vitro and in vivo study in mice

2014 ◽  
Vol 63 ◽  
pp. 114-123 ◽  
Author(s):  
Irina Surgucheva ◽  
Shuangteng He ◽  
Megan C. Rich ◽  
Ram Sharma ◽  
Natalia N. Ninkina ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
In Vivo Study

scholarly journals Neutrophil Extracellular Traps Facilitate Sympathoexcitation After Traumatic Brain Injury Via HMGB1/AP1 Signaling Pathway

2021 ◽  
Author(s):  
Kaixin Zhu ◽  
Xiaoxiang Hou ◽  
Xiaolin Qu ◽  
Wen Chen ◽  
Kun Chen ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Diffuse Axonal Injury ◽  
Neutrophil Extracellular Traps ◽  
Control Group ◽  
Extracellular Traps ◽  
Important Form

Abstract Background: Traumatic brain injury (TBI) usually accompanies with sympathetic excitation, and paradoxical sympathetic hyperactivity (PSH) may be detrimental to the prognosis of TBI sufferers. Neutrophils can form neutrophil extracellular traps (NETs) to get involved in the neuroinflammation after TBI. As an important form of NETs, HMGB1 were found to activate the expression of AP1, which can increase the formation of IL-1β in microglia. Considering that IL-1β is able to regulate sympathoexcitation, it is reasonable to infer that HMGB1/AP1 signaling plays an important role in sympathoexcitation after TBI. Methods: In this present study, rat model with diffuse axonal injury (DAI) was established. The existance of NETs and the expression level of HMGB1/AP1/IL-1β in the paraventricular nucleus (PVN) after DAI were examined by immunofluorescence and Western blot (WB). The role of HMGB1/AP1 in the activation of microglia, secretion of IL-1β and sympathoexcitaiton were identified in vitro. Moreover, stereotaxic injection of anti-HMGB1 or HMGB1 was conducted to further validate the effect of HMGB1/AP1 pathway on sympathoexcitation after TBI.Results: The indicators of sympathoexcitation, including mean arterial pressure and serum catecholamine, increased and peaked at 72 hours after TBI. The formation of NETs was observed in PVN after injury, whereas, no NETs were found in the control group. And meanwhile, levels of NETs in PVN were higher than that in the para-PVN tissues after the injury. In vitro experiments showed that HMGB1 can promote the activation of microglia as well as increase the expression of AP1 and IL-1β. In vivo experiments suggested HMGB1 have an impact on the expression of AP1 and IL-1β in the PVN, and further controlling the sympathoexcitation after TBI.Conclusion: NETs might mediate sympathoexcitation after TBI through microglial activation in the PVN in a HMGB1/AP1/IL-1β dependent way.

scholarly journals Posttraumatic Invasion of Monocytes across the Blood—Cerebrospinal Fluid Barrier

2011 ◽  
Vol 32 (1) ◽  
pp. 93-104 ◽  
Author(s):  
Joanna Szmydynger-Chodobska ◽  
Nathalie Strazielle ◽  
Jessica R Gandy ◽  
Timothy H Keefe ◽  
Brian J Zink ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Inflammatory Cells ◽  
Electron Microscopic ◽  
Injured Brain ◽  
Pathophysiological Role ◽  
Choroidal Epithelium ◽  
Epithelial Barriers ◽  
Vitro Model ◽  
A Site

The invasion of inflammatory cells occurring after ischemic or traumatic brain injury (TBI) has a detrimental effect on neuronal survival and functional recovery after injury. We have recently demonstrated that not only the blood-brain barrier, but also the blood-cerebrospinal fluid (CSF) barrier (BCSFB), has a role in posttraumatic recruitment of neutrophils. Here, we show that TBI results in a rapid increase in synthesis and release into the CSF of a major chemoattractant for monocytes, CCL2, by the choroid plexus epithelium, a site of the BCSFB. Using an in vitro model of the BCSFB, we also show that CCL2 is released across the apical and basolateral membranes of the choroidal epithelium, a pattern of chemokine secretion that promotes leukocyte migration across epithelial barriers. Immunohistochemical and electron microscopic analyses of choroidal tissue provide evidence for the movement of monocytes, sometimes in tandem with neutrophils, along the paracellular pathways between adjacent epithelial cells. These data further support the pathophysiological role of BCSFB in promoting the recruitment of inflammatory cells to the injured brain.

Role of innate inflammation in traumatic brain injury

2021 ◽  
Author(s):  
Sandrine Bourgeois-Tardif ◽  
Louis De Beaumont ◽  
José Carlos Rivera ◽  
Sylvain Chemtob ◽  
Alexander G Weil
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury

scholarly journals P88 Paroxysmal sympathetic storm and the role of beta-blockers in traumatic brain injury: a scoping review protocol

BJS Open ◽  
2021 ◽  
Vol 5 (Supplement_1) ◽  
Author(s):  
Stéphane Nguembu ◽  
Marco Meloni ◽  
Geneviève Endalle ◽  
Hugues Dokponou ◽  
Olaoluwa Ezekiel Dada ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Length Of Stay ◽  
Glasgow Coma Scale ◽  
Scoping Review ◽  
Beta Blockers ◽  
Clinical Signs ◽  
Sympathetic Hyperactivity ◽  
Paroxysmal Sympathetic Hyperactivity

Abstract Introduction Most cases of paroxysmal sympathetic hyperactivity (PSH) result from traumatic brain injury (TBI). Little is known about its pathophysiology and treatment, and several neuroprotective drugs are used including beta-blockers. The aim of our study is to collate existing evidence of the role of beta-blockers in the treatment of PSH. Method We will search MEDLINE, Web of Science, EMBASE, Cochrane, and Google Scholar. The search terms used will cover the following terms: “paroxysmal sympathetic hyperactivity”, “traumatic brain injury” and “beta-blockers.”: No language or geographical restrictions will be applied. Two independent co-authors will screen the titles and abstracts of each article following predefined inclusion and exclusion criteria. If there is a conflict the two reviewers will find a consensus and if they cannot a third co-author will decide. Using a pre-designed and pre-piloted data extraction form, data from each included citation will be collected (authors identification, study type, TBI severity, type of beta-blockers used, dosage of the drug, clinical signs of PSH, Glasgow Coma Scale, Glasgow Outcome Scale, mortality, morbidity and length of stay). Simple descriptive data analyses will be performed and the results will be presented both in a narrative and tabular form. Results The effectiveness of beta-blockers in post-TBI PHS will be evaluated through clinical signs of PHS(increased heart rate, respiratory rate, temperature, blood pressure, and sweating), Glasgow Coma Scale, and Glasgow Outcome Scale. mortality, morbidity and length of stay. Conclusion At the end of this scoping review we will design a systematic review with metaanalysis if there are a reasonable number of studies otherwise we will design a randomized controlled trial.

Polydatin alleviates traumatic brain injury: Role of inhibiting ferroptosis

2021 ◽  
Vol 556 ◽  
pp. 149-155
Author(s):  
Lu Huang ◽  
Shulei He ◽  
Qing Cai ◽  
Fei Li ◽  
Siwei Wang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury

scholarly journals Creatine Supplementation and Brain Health

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 586 ◽  
Author(s):  
Hamilton Roschel ◽  
Bruno Gualano ◽  
Sergej M. Ostojic ◽  
Eric S. Rawson
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Function ◽  
Cognitive Processing ◽  
Brain Function ◽  
Creatine Supplementation ◽  
Short Review ◽  
Future Research ◽  
Brain Health

There is a robust and compelling body of evidence supporting the ergogenic and therapeutic role of creatine supplementation in muscle. Beyond these well-described effects and mechanisms, there is literature to suggest that creatine may also be beneficial to brain health (e.g., cognitive processing, brain function, and recovery from trauma). This is a growing field of research, and the purpose of this short review is to provide an update on the effects of creatine supplementation on brain health in humans. There is a potential for creatine supplementation to improve cognitive processing, especially in conditions characterized by brain creatine deficits, which could be induced by acute stressors (e.g., exercise, sleep deprivation) or chronic, pathologic conditions (e.g., creatine synthesis enzyme deficiencies, mild traumatic brain injury, aging, Alzheimer’s disease, depression). Despite this, the optimal creatine protocol able to increase brain creatine levels is still to be determined. Similarly, supplementation studies concomitantly assessing brain creatine and cognitive function are needed. Collectively, data available are promising and future research in the area is warranted.

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