INT12720
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
In turn, these substances bind kappa-opioid receptors expressed in GM-CSF-activated macrophage-like stromal cells and seem to stimulate IL-1. | |||||||||||||||
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Although barely detectable in the normal brain, IL-1 is dramatically upregulated during neuroinflammation, and also displays peaks of expression in the brain during development, as well as following the induction of long-term potentiation. | |||||||||||||||
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Treatment with taurine and niacin attenuated the BL-induced increases in proinflammatory cytokines such as IL-1alpha, TNF-alpha, IL-6, and TGF-beta in BALF and lung hydroxyproline content of the mice in BL + TN groups. | |||||||||||||||
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Reverse transcription-polymerase chain reaction analysis of total RNA from whole lung was performed to assess the induction of TNF-alpha and IL-1 mRNAs as markers of NF-kappaB activation. | |||||||||||||||
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In response to homeostatic threats in mammals, increased IL-1 levels activate the hypothalamo-pituitary-adrenal (HPA) axis and are central to elicitation of sickness behaviors. | |||||||||||||||
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Experimentally induced elevations of IL-1? | |||||||||||||||
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The initial stimulus for elevation of IL-1 in AD is likely the result of exposure of microglia to injured neurons, ? | |||||||||||||||
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This pattern of expression was further extended to animal models of CNS injury where parenchymal IL-1 mRNA and protein levels are elevated in experimental models of ischemia, excitotoxicity, infection and traumatic brain injury in rodents. | |||||||||||||||
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Furthermore, increased IL-1 has been detected in CSF samples in MS, Parkinson's and Creutzfeldt-Jakob disease (CJD) [26-28]. | |||||||||||||||
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Also, injection of lipopolysaccharide (LPS), a potent inducer of IL-1? | |||||||||||||||
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IL-1 elevations became closely tied to AD pathogenesis soon after the discovery of prominent neuroinflammation in AD brain. | |||||||||||||||
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As highlighted above, IL-1 elevation may potentiate plaque degradation by enhancing microglial activation and phagocytic activity, as well as seeding of peripheral phagocytic cells to areas of plaque deposition [44]. | |||||||||||||||
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By feeding back upon itself, small localized elevations in IL-1 may be sufficient to drive potent neuroinflammatory changes in the brain. | |||||||||||||||
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Moreover, the result of high circulating TNF and IL-1? | |||||||||||||||
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-inhibitor (0,1 mM) followed IL-1? | |||||||||||||||
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It is also conceivable that the unavoidable injury caused by cannula implantation (even after the several days of convalescence) may have promoted the activation of local inflammatory factors, thereby influencing the impact of subsequently administered IL-1? | |||||||||||||||
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levels.30 In agreement with this finding, the reduction of hippocampal neurogenesis normally associated with chronic stressor exposure was prevented in IL-1 type 1 receptor knockout mice.31 Likewise, alterations of hippocampal neurogenesis were reported in adult transgenic mice over-expressing IL-6,31 and administration of the bacterial endotoxin lipopolysaccharide (LPS) suppressed neurogenesis while concomitantly elevating IL-1? | |||||||||||||||
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As a first step to determining the utility of the IL-1 CIA model as a drug screen, we examined the ability of various known anti-inflammatory and anti-arthritic drugs to modify the IL-1 mediated enhancement of CIA in both rats and mice. | |||||||||||||||
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This intervention did not affect IL-1beta gene transcription but prevented the increase in IL-1beta plasma levels. | |||||||||||||||
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Reverse transcription-polymerase chain reaction analysis of total RNA from whole lung was performed to assess the induction of TNF-alpha and IL-1 mRNAs as markers of NF-kappaB activation. | |||||||||||||||
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