Potential mechanisms of interleukin-1 involvement in cerebral ischaemia

Touzani, Omar; Boutin, Hervé; Chuquet, Julien; Rothwell, Nancy J.

doi:10.1016/s0165-5728(99)00202-7

Cited by 216 publications

(140 citation statements)

References 89 publications

Supporting

Mentioning

124

Contrasting

Unclassified

Order By: Relevance

“…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: 92%

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)

View full text Add to dashboard Cite

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.

show abstract

Section: Microdialysis In Vivosupporting

confidence: 92%

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)

View full text Add to dashboard Cite

show abstract

“…Secondly, fever, a cardinal feature of the immune response in infection, is associated with worse neurologic outcome after stroke (Azzimondi et al, 1995;Reith et al, 1996). Thirdly, the cytokines secreted by leukocytes during the effector phase of an immune response might be toxic to neurons and glia (Barone et al, 1997;Hanisch et al, 1996;Touzani et al, 1999). Finally, because the bacterial products associated with infection (i.e.…”

Section: Discussionmentioning

confidence: 99%

Sensitization to Brain Antigens after Stroke is Augmented by Lipopolysaccharide

Becker

Kindrick

Lester

et al. 2005

J Cereb Blood Flow Metab

113

158

View full text Add to dashboard Cite

After stroke, the blood-brain barrier is transiently disrupted, allowing leukocytes to enter the brain and brain antigens to enter the peripheral circulation. This encounter of normally sequestered brain antigens by the systemic immune system could therefore present an opportunity for an autoimmune response to brain to occur after stroke. In this study, we assessed the immune response to myelin basic protein (MBP) in animals subjected to middle cerebral artery occlusion (MCAO). Some animals received an intraperitoneal injection of lipopolysaccharide (LPS; 1 mg/kg) at reperfusion to stimulate a systemic inflammatory response. At 1 month after MCAO, animals exposed to LPS were more likely to be sensitized to MBP (66.7% versus 22.2%; P ¼ 0.007) and had more profound and persistent neurologic deficits than non-LPS-treated animals. Exposure to LPS was associated with increased expression of the costimulatory molecule B7.1 early after stroke onset (P ¼ 0.009) and increased brain atrophy 1 month after MCAO (P ¼ 0.03). These data suggest that animals subjected to a systemic inflammatory insult at the time of stroke are predisposed to develop an autoimmune response to brain, and that this response is associated with worse outcome. These data may partially explain why patients who become infected after stroke experience increased morbidity.

show abstract

“…Although the mechanisms of chemokinemediated neuronal death are not well defined at present, previous studies on transient forebrain ischemia suggest that early production of inflammatory mediators in activated microglial cells, including IL-1␤, TNF-␣, and NO, may contribute to ischemic neuronal death (Sairanen et al, 1997;Uno et al, 1997;Yamashita et al, 2000). As a matter of fact, ischemic brain damage is attenuated by administration of anti-inflammatory drugs (Yrjanheikki et al, 1998;Arvin et al, 2002;Wang et al, 2003), but potentiated by maneuvers enhancing IL-1␤, TNF-␣, and NO (Barone et al, 1997;Dirnagl et al, 1999;Touzani et al, 1999;Zhao et al, 2003). We found free radical production in the CA1 neurons 2 d as well as 2 h after TFI (Park et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Free Radical Production in CA1 Neurons Induces MIP-1α Expression, Microglia Recruitment, and Delayed Neuronal Death after Transient Forebrain Ischemia

Wang

Park²,

Kim³

et al. 2008

J. Neurosci.

View full text Add to dashboard Cite

Several studies report microglial accumulation and activation in the CA1 area in response to transient forebrain ischemia (TFI). Here we examine the possibility that free radicals and chemokines mediate the transient activation of microglia. Free radicals are produced primarily in CA1 pyramidal neurons within 2 h of TFI. Administration of trolox, a vitamin E analog, led to the inhibition of free radical production and recruitment of microglia in the CA1 area. In addition, intrahippocampal injection of Fe 2ϩ triggered free radical production in CA1 neurons, followed by the recruitment and activation of microglial cells into this area. TFI-induced expression of macrophage inflammatory protein-1␣ (MIP-1␣) was increased in CA1 neurons before microglial recruitment, and blocked by trolox. Moreover, the MIP-1␣ level was upregulated in cultured hippocampal neurons exposed to Fe 2ϩ , suggesting an essential role of free radicals in TFIinduced expression of MIP-1␣. Intracerebroventricular injection of vMIP-2 (viral macrophage inflammatory protein-2), a broadspectrum peptide antagonist of chemokine receptors, attenuated microglial recruitment and delayed CA1 neuronal degeneration after TFI. Our data suggest that free radicals produced in CA1 neurons contribute to the recruitment and activation of microglia and neurodegeneration through MIP-1␣ expression.

show abstract

Potential mechanisms of interleukin-1 involvement in cerebral ischaemia

Cited by 216 publications

References 89 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

Sensitization to Brain Antigens after Stroke is Augmented by Lipopolysaccharide

Free Radical Production in CA1 Neurons Induces MIP-1α Expression, Microglia Recruitment, and Delayed Neuronal Death after Transient Forebrain Ischemia

Contact Info

Product

Resources

About