The Role of Inflammation and Cytokines in Brain Injury

Arvin, B. Mak; Neville, Lewis F.; Barone, Frank C.; Feuerstein, Giora

doi:10.1016/0149-7634(95)00026-7

Cited by 372 publications

(197 citation statements)

References 102 publications

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“…This observation is in accordance with previous studies, which have shown increased expression of IL-1ß in the acute phase following traumatic brain injury [12,21,22]. IL-1ß is a pluripotent cytokine and plays a key role in the inflammatory cascade [3,48]. It has been reported that IL-1ß acts as a mediator in the inflammatory response and induces the expression of neuroprotectant-and neurotrophic factors in a traumatised brain [30].…”

Section: Microdialysis In Vivosupporting

confidence: 81%

“…Conclusions Cerebral microdialysis allows measurement of cytokine secretion in the ECF of brain tissue in rats. [3,8,9,13,16,17,28,[41][42][43]. The exact contribution of these substances to local tissue damage is still not fully understood.…”

Section: Methodsmentioning

confidence: 99%

“…This pluripotent, pro-inflammatory cytokine participates in a complex network of signalling molecules and seems to be one of the most important factors in the propagation and maintenance of the inflammatory cascade after TBI, being responsible for enhancing the activation of T-cells [3,8,20,27]. IL-1 ß belongs to the IL-1 family which has three wellknown endogenous ligands, two agonists, IL-1α and IL-1 ß, and one IL-1 receptor antagonist [23].…”

Section: Methodsmentioning

confidence: 99%

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Cerebral microdialysis of interleukin (IL)-1ß and IL-6: extraction efficiency and production in the acute phase after severe traumatic brain injury in rats

Folkersma

Brevé

Tilders

et al. 2008

Acta Neurochir (Wien)

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Background As a research tool, cerebral microdialysis might be a useful technique in monitoring the release of cytokines into the extracellular fluid (ECF) following traumatic brain injury (TBI). We established extraction efficiency of Interleukin(IL)-1ß and Interleukin(IL)-6 by an in vitro microdialysis-perfusion system, followed by in vivo determination of the temporal profile of extracellular fluid cytokines after severe TBI in rats. Materials and methodsIn vitro experiments using a polyether sulfon (PES) microdialysis probe especially developed for recovery of macromolecules such as cytokines, were carried out to establish the extraction efficiency of IL-1ß and IL-6 from artificial cerebrospinal fluid (CSF) with defined IL-1ß and IL-6 concentrations. In vivo experiments in which rats were subjected to TBI or sham and microdialysis samples were collected from the parietal lobe for measurement of cytokines. Findings The extraction efficiency was maximal 6.05% (range, 5.97-6.13%) at 0.5 µl/min −1 and decreased at higher flow rates. Both cytokines were detectable in the dialysates. Highest IL-1ß levels were found within 200 min, highest IL-6 concentrations were detected at later intervals (200-400 min). No differences were found between the TBI and control groups. Conclusions Cerebral microdialysis allows measurement of cytokine secretion in the ECF of brain tissue in rats.

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Section: Microdialysis In Vivosupporting

confidence: 81%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Cerebral microdialysis of interleukin (IL)-1ß and IL-6: extraction efficiency and production in the acute phase after severe traumatic brain injury in rats

Folkersma

Brevé

Tilders

et al. 2008

Acta Neurochir (Wien)

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“…It is well established that inflammation represents a key event in stroke, contributing to brain injury and perhaps modulating some of the identified pathways of cell death (10). NF-B is a ubiquitous transcription factor that mediates a variety of proinflammatory responses (11).…”

mentioning

confidence: 99%

Tauroursodeoxycholic acid reduces apoptosis and protects against neurological injury after acute hemorrhagic stroke in rats

Rodrigues

Solá

Nan

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

186

128

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Tauroursodeoxycholic acid (TUDCA), an endogenous bile acid, modulates cell death by interrupting classic pathways of apoptosis. Intracerebral hemorrhage (ICH) is a devastating acute neurological disorder, without effective treatment, in which a significant loss of neuronal cells is thought to occur by apoptosis. In this study, we evaluated whether TUDCA can reduce brain injury and improve neurological function after ICH in rats. Administration of TUDCA before or up to 6 h after stereotaxic collagenase injection into the striatum reduced lesion volumes at 2 days by as much as 50%. Apoptosis was Ϸ50% decreased in the area immediately surrounding the hematoma and was associated with a similar inhibition of caspase activity. These changes were also associated with improved neurobehavioral deficits as assessed by rotational asymmetry, limb placement, and stepping ability. Furthermore, TUDCA treatment modulated expression of certain Bcl-2 family members, as well as NF-B activity. In addition to its protective action at the mitochondrial membrane, TUDCA also activated the Akt-1͞protein kinase B␣ survival pathway and induced Bad phosphorylation at Ser-136. In conclusion, reduction of brain injury underlies the wide-range neuroprotective effects of TUDCA after ICH. Thus, given its clinical safety, TUDCA may provide a potentially useful treatment in patients with hemorrhagic stroke and perhaps other acute brain injuries associated with cell death by apoptosis.

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“…It is therefore of paramount importance that the development of edema is inhibited following TBI. Although a number of studies have investigated the role of classical inflammation in edema formation following TBI, 32,33 to date few studies have examined the role of neurogenic inflammation. Nimmo et al 7 were among the first to do so, by demonstrating that chronic administration of capsaicin prior to TBI significantly attenuated BBB opening, edema formation, and the development of both motor and cognitive deficits.…”

Section: Edemamentioning

confidence: 99%

Substance P Antagonists as a Therapeutic Approach to Improving Outcome Following Traumatic Brain Injury

Vink

Heuvel

2010

Neurotherapeutics

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Summary:Although a number of secondary injury factors are known to contribute to the development of morphological injury and functional deficits following traumatic brain injury, accumulating evidence has suggested that neuropeptides, and in particular substance P, may play a critical role. Substance P is released early following acute injury to the CNS as part of a neurogenic inflammatory response. In so doing, it facilitates an increase in the permeability of the bloodbrain barrier and the development of vasogenic edema. At the cellular level, substance P has been shown to directly result in neuronal cell death; functionally, substance P has been implicated in learning and memory, mood and anxiety, stress mechanisms, emotion-processing, migraine, emesis, pain, and seizures, all of which may be adversely affected after brain injury. Inhibition of post-traumatic substance P activity, either by preventing release or by antagonism of the neurokinin-1 receptor, has consistently resulted in a profound decrease in development of edema and marked improvements in functional outcome. This review summarizes the current evidence supporting a role for substance P in acute brain injury.

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The Role of Inflammation and Cytokines in Brain Injury

Cited by 372 publications

References 102 publications

Cerebral microdialysis of interleukin (IL)-1ß and IL-6: extraction efficiency and production in the acute phase after severe traumatic brain injury in rats

Cerebral microdialysis of interleukin (IL)-1ß and IL-6: extraction efficiency and production in the acute phase after severe traumatic brain injury in rats

Tauroursodeoxycholic acid reduces apoptosis and protects against neurological injury after acute hemorrhagic stroke in rats

Substance P Antagonists as a Therapeutic Approach to Improving Outcome Following Traumatic Brain Injury

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