INT25610

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Context Info
Confidence 0.67
First Reported 1988
Last Reported 2011
Negated 2
Speculated 2
Reported most in Body
Documents 136
Total Number 138
Disease Relevance 104.43
Pain Relevance 43.86

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

Anatomy Link Frequency
macrophages 13
joints 8
monocytes 7
fibroblasts 6
brain 5
Il1 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 2836 100.00 Very High Very High Very High
cytokine 2819 100.00 Very High Very High Very High
Arthritis 2819 100.00 Very High Very High Very High
antagonist 243 100.00 Very High Very High Very High
cINOD 308 99.82 Very High Very High Very High
substance P 119 99.78 Very High Very High Very High
Hippocampus 165 99.64 Very High Very High Very High
Central nervous system 662 99.52 Very High Very High Very High
opioid receptor 13 99.52 Very High Very High Very High
agonist 138 99.48 Very High Very High Very High
Disease Link Frequency Relevance Heat
Arthritis 3193 100.00 Very High Very High Very High
INFLAMMATION 3160 100.00 Very High Very High Very High
Injury 784 100.00 Very High Very High Very High
Targeted Disruption 616 100.00 Very High Very High Very High
Infection 550 100.00 Very High Very High Very High
Crystal Associated Disease 379 100.00 Very High Very High Very High
Cancer 326 100.00 Very High Very High Very High
Necrosis 218 100.00 Very High Very High Very High
Granuloma 186 100.00 Very High Very High Very High
Sepsis 126 100.00 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
However, an upregulated lung expression for TNF-alpha and IL-1 receptors was observed in C57Bl/6J-sensitive animals only.
Positive_regulation (upregulated) of Gene_expression (expression) of IL-1 in lung
1) Confidence 0.67 Published 2004 Journal Am. J. Physiol. Lung Cell Mol. Physiol. Section Abstract Doc Link 15321784 Disease Relevance 0.47 Pain Relevance 0.43
Nonsteroidal anti-inflammatory drugs are not stimulating IL-1 production but are, in fact, relieving inhibition of the thymocyte IL-1 assay caused by the presence of prostaglandins.
Neg (not) Positive_regulation (stimulating) of Gene_expression (production) of IL-1 in thymocyte associated with inflammation and cinod
2) Confidence 0.65 Published 1988 Journal Cell. Immunol. Section Abstract Doc Link 2968844 Disease Relevance 0.10 Pain Relevance 0.10
Furthermore, LPS-induced IL-1 production by macrophages (in the absence of added beta-endorphin) was also partially inhibited following treatment with naloxone, suggesting that opioids derived from activated macrophages may also modulate IL-1 generation and secretion.
Positive_regulation (induced) of Gene_expression (production) of IL-1 in macrophages associated with narcan and opioid
3) Confidence 0.61 Published 1989 Journal Int. Immunol. Section Abstract Doc Link 2535139 Disease Relevance 0 Pain Relevance 0.31
Naloxone, a competitive inhibitor of beta-endorphin opioid receptor interactions, abrogated the enhancing effects of beta-endorphin on LPS-induced IL-1 production.
Positive_regulation (induced) of Gene_expression (production) of IL-1 associated with narcan and opioid receptor
4) Confidence 0.61 Published 1989 Journal Int. Immunol. Section Abstract Doc Link 2535139 Disease Relevance 0 Pain Relevance 0.30
However, over a wide range of concentrations (10(-6)-10(-14) M) beta-endorphin potentiated lipopolysaccharide (LPS)- or silica-induced production of intracellular and extracellular IL-1.
Positive_regulation (induced) of Gene_expression (production) of IL-1
5) Confidence 0.61 Published 1989 Journal Int. Immunol. Section Abstract Doc Link 2535139 Disease Relevance 0 Pain Relevance 0.26
The elevation of IL-1 expression following a diverse array of acute brain injuries coupled with its ability to elicit diverse inflammatory changes as previously discussed, suggests that it may contribute to the pathogenesis of CNS injury.
Positive_regulation (elevation) of Gene_expression (expression) of IL-1 in brain associated with inflammation, injury, central nervous system and brain injury
6) Confidence 0.60 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2335091 Disease Relevance 1.14 Pain Relevance 0.39
Microglia chronically exposed to these stimuli during the course of disease likely mount sustained elevations in IL-1 and drive a self-perpetuating cycle of IL-1 overexpression in the brain parenchyma leading to chronic neuroinflammation [45].
Positive_regulation (overexpression) of Gene_expression (overexpression) of IL-1 in parenchyma associated with disease
7) Confidence 0.60 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2335091 Disease Relevance 0.70 Pain Relevance 0.07
Increased expression of IL-1RII, the biologically inactive "decoy" IL-1 receptor, has been demonstrated following injection of IL-1?
Positive_regulation (Increased) of Gene_expression (expression) of IL-1RII
8) Confidence 0.60 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2335091 Disease Relevance 1.03 Pain Relevance 0.11
For example, chronic hippocampal overexpression of human IL-1?
Positive_regulation (overexpression) of Gene_expression (overexpression) of IL-1
9) Confidence 0.60 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2335091 Disease Relevance 0.85 Pain Relevance 0.26
Increased IL-1 expression in reactive microglia surrounding amyloid plaques provided the initial indication that IL-1 may be associated with AD pathogenesis [17].
Positive_regulation (Increased) of Gene_expression (expression) of IL-1 in plaques associated with alzheimer's dementia and amyloid plaque
10) Confidence 0.60 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2335091 Disease Relevance 1.59 Pain Relevance 0.24
Initial evidence that IL-1 may play a key role in local brain tissue reactions came from demonstrations of elevated IL-1 expression in a diverse array of CNS diseases.
Positive_regulation (elevated) of Gene_expression (expression) of IL-1 in brain associated with central nervous system and disease
11) Confidence 0.60 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2335091 Disease Relevance 1.26 Pain Relevance 0.33
In a second set of experiments, HUVEC were pre-treated with IL-1?
Positive_regulation (treated) of Gene_expression (with) of IL-1
12) Confidence 0.49 Published 2006 Journal J Inflamm (Lond) Section Body Doc Link PMC1435878 Disease Relevance 0.42 Pain Relevance 0
These morphological characteristics and pattern of distribution closely resemble that ordinarily reported.37 Although no significant treatment effects were observed in the middle and caudal levels of the hippocampus, there was a trend towards a cytokine-induced reduction of BrdU labelling, such that in the middle hippocampal region, IL-1?
Positive_regulation (induced) of Gene_expression (reduction) of IL-1 in hippocampus associated with hippocampus and cytokine
13) Confidence 0.49 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2695223 Disease Relevance 0.14 Pain Relevance 0.22
When NF161 or NF177 were added simultaneously with IL-1?
Positive_regulation (simultaneously) of Gene_expression (added) of IL-1
14) Confidence 0.49 Published 2006 Journal J Inflamm (Lond) Section Body Doc Link PMC1435878 Disease Relevance 0.34 Pain Relevance 0.21
reduced hippocampal neurogenesis in rodents, and this effect was dependent upon endogenous IL-1?
Positive_regulation (upon) of Gene_expression (dependent) of IL-1 associated with neurodegenerative disease
15) Confidence 0.49 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2695223 Disease Relevance 1.37 Pain Relevance 0.36
Further dilutions of the drug-treated supernatants gave thymocyte proliferation responses which were indistinguishable from control cultures and, correspondingly, had identical values for IL-1 production.
Positive_regulation (values) of Gene_expression (production) of IL-1 in thymocyte
16) Confidence 0.47 Published 1988 Journal Cell. Immunol. Section Abstract Doc Link 2968844 Disease Relevance 0 Pain Relevance 0
The role of prostaglandins in the regulation of lipopolysaccharide (LPS)-induced interleukin-1 (IL-1) production by murine C3H/HeN resident peritoneal macrophages was studied.
Positive_regulation (-induced) of Gene_expression (production) of IL-1 in peritoneal macrophages
17) Confidence 0.47 Published 1988 Journal Cell. Immunol. Section Abstract Doc Link 2968844 Disease Relevance 0 Pain Relevance 0
The present study examined the hypothesis that IL-1 signaling is also involved in pain sensitivity under normal, non-inflammatory states, using three mouse models of impaired IL-1 signaling: targeted deletion of the IL-1 receptor type I or the IL-1 receptor accessory protein, and transgenic over-expression of IL-1 receptor antagonist within the brain and spinal cord.
Positive_regulation (over-expression) of Gene_expression (over-expression) of IL-1 in spinal cord associated with targeted disruption, pain, inflammation, antagonist and spinal cord
18) Confidence 0.45 Published 2003 Journal Pain Section Abstract Doc Link 12927619 Disease Relevance 1.02 Pain Relevance 0.73
Thus, beta-endorphin-opioid receptor interactions result in enhanced production of immunomodulators such as IL-1.
Positive_regulation (enhanced) of Gene_expression (production) of IL-1 associated with opioid receptor
19) Confidence 0.44 Published 1989 Journal Int. Immunol. Section Abstract Doc Link 2535139 Disease Relevance 0 Pain Relevance 0.30
However, over a wide range of concentrations (10(-6)-10(-14) M) beta-endorphin potentiated lipopolysaccharide (LPS)- or silica-induced production of intracellular and extracellular IL-1.
Positive_regulation (potentiated) of Gene_expression (production) of IL-1
20) Confidence 0.44 Published 1989 Journal Int. Immunol. Section Abstract Doc Link 2535139 Disease Relevance 0 Pain Relevance 0.26

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