The Effect of Traumatic Brain Injury Upon the Concentration and Expression of Interleukin-1 and Interleukin-10 in the Rat

Kamm, Keira; VanderKolk, Wayne E.; Davis, Alan T.; Lawrence, Chuck; Jonker, Mark A.

doi:10.1097/00005373-200412000-00098

Cited by 48 publications

(66 citation statements)

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“…Given the delay of the signal which is in the present setup approximately 60-90 min, it seems that IL-1ß that is present in the first sample is supposed to be secreted short after placement of the dialysis probe in healthy or traumatised brain tissue. 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].…”

Section: Microdialysis In Vivosupporting

confidence: 93%

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: 93%

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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“…The time course of release of TNF-α has is remarkably consistent across experimental paradigms of focal TBI in rodents (closed cortical impact, fluid percussion, or stab wound injury), with detectable levels at 1 h post-injury, maximal concentration at 3-8 h, and a decline in release by 24 h within the brain [162,163]. In diffuse injury models, serum levels of TNF-α rise within 24 h with an absence of expression in brain tissue, suggesting that diffuse injury induces a different immune response [164]. Similar to TNF-α, IL-6 has shown to play a role in neuroinflammation that is detected by 1 h postinjury in animal models, followed by a peak concentration between 2 and 8 h [153,165,166].…”

Section: Animal Models Of T/hs and Tbimentioning

confidence: 62%

The Acute Inflammatory Response in Trauma /Hemorrhage and Traumatic Brain Injury: Current State and Emerging Prospects

Namas¹,

Ghuma²,

Hermus

et al. 2008

Libyan Journal of Medicine

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Abstract; Traumatic injury/hemorrhagic shock (T/HS) elicits an acute inflammatory response that may result in death. Inflammation describes a coordinated series of molecular, cellular, tissue, organ, and systemic responses that drive the pathology of various diseases including T/HS and traumatic brain injury (TBI). Inflammation is a finely tuned, dynamic, highly-regulated process that is not inherently detrimental, but rather required for immune surveillance, optimal post-injury tissue repair, and regeneration. The inflammatory response is driven by cytokines and chemokines and is partially propagated by damaged tissue-derived products (Damage-associated Molecular Patterns; DAMP's). DAMPs perpetuate inflammation through the release of pro-inflammatory cytokines, but may also inhibit anti-inflammatory cytokines. Various animal models of T/HS in mice, rats, pigs, dogs, and non-human primates have been utilized in an attempt to move from bench to bedside. Novel approaches, including those from the field of systems biology, may yield therapeutic breakthroughs in T/HS and TBI in the near future.

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“…Conversely, the fundamental mechanisms underlying secondary damage in TBI include inflammation, oxygen free radicals, brain edema formation and neuronal apoptosis (4). In particular, previous studies have demonstrated that tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 are crucial pro-inflammatory cytokines following trauma (5)(6)(7). Although the potential effects of TNF-α, IL-1β and IL-6 in human patients with TBI have yet to be elucidated, evidence from animal models has revealed that upregulated expression levels of the aforementioned cytokines are harmful, whereas their attenuation may alleviate tissue damage as well as brain edema, thereby improving the functional outcomes of patients with TBI (8).…”

Section: Introductionmentioning

confidence: 99%

Hsp70 inducer, 17-allylamino-demethoxygeldanamycin, provides neuroprotection via anti-inflammatory effects in a rat model of traumatic brain injury

Wang

Zhou

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Traumatic brain injury (TBI) is the predominant cause of mortality in young adults and children living in China. TBI induces inflammatory responses; in addition, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 are important pro-inflammatory cytokines. Considering the observation that Hsp-70 overexpression can exert neuroprotection, identifying a drug that is able to induce the upregulation of Hsp70 has the potential to be a promising therapy for the treatment of neurological diseases. Thus, the present study assessed the clinical effectiveness of an anticancer drug and Hsp70 activator, 17-allylamino-demethoxygeldanamycin (17-AAG), to evaluate its potential as a treatment for patients with TBI. The aim of present study was to determine the neuroprotective effects of 17-AAG following trauma and to investigate the underlying mechanisms of action. To establish rat models, rats were subjected to a controlled cortical impact injury and randomly divided into vehicle or 17-AAG groups. In the 17-AAG group, rats were administered with an intraperitoneal injection of 17-AAG (80 mg/kg) immediately following the establishment of TBI. The motor function was measured using Neurologic Severity Score, and neuronal death was evaluated using immunofluorescence. The expression levels of GLT-1, Bcl-2 and Hsp-70 were detected by western blot analysis and the expression levels of inflammatory cytokines were quantified using ELISA. The present study determined that 17-AAG significantly reduced brain edema and motor neurological deficits (P<0.05), in addition to increasing neuronal survival. The aforementioned findings are associated with a downregulation of the expression levels of pro-inflammatory cytokines TNF-α, IL-1β and IL-6. Conversely, no significant changes of glutamate transporter-1 expression were observed. The present results suggest that 17-AAG treatment may provide a neuroprotective effect by reducing inflammation following TBI. IntroductionTraumatic brain injury (TBI) is the leading cause of mortality in young adults and children living in China (1). Head trauma has numerous consequences in the brain, including axonal damage, microvascular alterations and blood-brain barrier disruption (2). The aforementioned outcomes are a result of both primary and secondary mechanisms following injury (3). Primary damage is a result of mechanical factors occurring immediately following trauma. Conversely, the fundamental mechanisms underlying secondary damage in TBI include inflammation, oxygen free radicals, brain edema formation and neuronal apoptosis (4). In particular, previous studies have demonstrated that tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 are crucial pro-inflammatory cytokines following trauma (5-7). Although the potential effects of TNF-α, IL-1β and IL-6 in human patients with TBI have yet to be elucidated, evidence from animal models has revealed that upregulated expression levels of the aforementioned cytokines are harmful, whereas their attenuation may alleviate tissue ...

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The Effect of Traumatic Brain Injury Upon the Concentration and Expression of Interleukin-1 and Interleukin-10 in the Rat

Cited by 48 publications

References 0 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

The Acute Inflammatory Response in Trauma /Hemorrhage and Traumatic Brain Injury: Current State and Emerging Prospects

Hsp70 inducer, 17-allylamino-demethoxygeldanamycin, provides neuroprotection via anti-inflammatory effects in a rat model of traumatic brain injury

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