INT142949

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Context Info
Confidence 0.71
First Reported 2006
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 27
Total Number 27
Disease Relevance 26.17
Pain Relevance 5.58

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

cell adhesion (FPR2) plasma membrane (FPR2) signal transducer activity (FPR2)
Anatomy Link Frequency
alveolar macrophages 6
blood 3
neutrophils 2
macrophages 1
neurons 1
FPR2 (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 672 100.00 Very High Very High Very High
corticosteroid 713 99.40 Very High Very High Very High
dexamethasone 483 99.40 Very High Very High Very High
cytokine 72 98.08 Very High Very High Very High
chemokine 2 97.56 Very High Very High Very High
Root ganglion neuron 1 94.44 High High
Pain 1 82.76 Quite High
dorsal root ganglion 1 81.92 Quite High
Analgesic 3 81.44 Quite High
opioid receptor 1 80.00 Quite High
Disease Link Frequency Relevance Heat
Asthma 2323 100.00 Very High Very High Very High
INFLAMMATION 677 100.00 Very High Very High Very High
Occupational Lung Diseases 851 99.76 Very High Very High Very High
Targeted Disruption 28 99.68 Very High Very High Very High
Cold Sores 2 99.32 Very High Very High Very High
Herpes Simplex Virus 1 99.12 Very High Very High Very High
Infection 86 95.84 Very High Very High Very High
Ganglion Cysts 28 94.24 High High
Inflammatory Bowel Disease 24 94.08 High High
Pulmonary Disease 46 90.44 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These results are in line with the current observation of reduced basal and LPS-stimulated production of LXA4 from alveolar macrophages of patients with severe asthma.
Gene_expression (production) of LXA4 in alveolar macrophages associated with asthma
1) Confidence 0.71 Published 2010 Journal Respir Res Section Body Doc Link PMC2894769 Disease Relevance 1.16 Pain Relevance 0
Using a similar method as our study to distinguish severe from non-severe asthma, a deficiency in both baseline and divalent cation ionophore-stimulated production of LXA4 in whole blood of patients with severe asthma compared to moderate asthma was established, while the production of cysteinyl-leukotrienes and LTB4 were increased[9].
Gene_expression (production) of LXA4 in blood associated with asthma
2) Confidence 0.71 Published 2010 Journal Respir Res Section Body Doc Link PMC2894769 Disease Relevance 1.38 Pain Relevance 0.14
The possibility that dysregulation of the balance among these arachidonic acid products might contribute to the persistent inflammation in severe asthma has been supported by the demonstration of an increased generation of cysteinyl-leukotrienes with impaired biosynthesis of lipoxin A4 (LXA4) from whole blood of patients with severe asthma compared to non-severe asthma patients[9].
Gene_expression (biosynthesis) of LXA4 in blood associated with asthma and inflammation
3) Confidence 0.71 Published 2010 Journal Respir Res Section Body Doc Link PMC2894769 Disease Relevance 1.31 Pain Relevance 0.31
The possibility that dysregulation of the balance among these arachidonic acid products might contribute to the persistent inflammation in severe asthma has been supported by the demonstration of an increased generation of cysteinyl-leukotrienes with impaired biosynthesis of lipoxin A4 (LXA4) from whole blood of patients with severe asthma compared to non-severe asthma patients[9].
Gene_expression (biosynthesis) of lipoxin A4 in blood associated with asthma and inflammation
4) Confidence 0.71 Published 2010 Journal Respir Res Section Body Doc Link PMC2894769 Disease Relevance 1.31 Pain Relevance 0.31
The LXA4 production induced by LPS is shown as the increment in LXA4 above baseline (Figure 1B).
Gene_expression (production) of LXA4
5) Confidence 0.71 Published 2010 Journal Respir Res Section Body Doc Link PMC2894769 Disease Relevance 0.95 Pain Relevance 0.06
G-RFP is a recombinant VSV derived from the cDNA of VSV Indiana, in which the G gene is replaced with the Ds-Red (RFP) gene.
Gene_expression (replaced) of RFP
6) Confidence 0.65 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2965769 Disease Relevance 0.47 Pain Relevance 0
There was a small but significant increase in LPS-induced LXA4 levels in all three groups (Figure 1B), with the lowest amounts in severe compared to non-severe asthma (p < 0.01) and to normal subjects (p < 0.001).
Gene_expression (levels) of LXA4 associated with asthma
7) Confidence 0.62 Published 2010 Journal Respir Res Section Body Doc Link PMC2894769 Disease Relevance 0.94 Pain Relevance 0.03
Indeed, in macrophages from severe asthma, this pro-inflammatory ratio favouring LTB4 over LXA4 was further unbalanced by dexamethasone.
Gene_expression (favouring) of LXA4 in macrophages associated with asthma, inflammation and dexamethasone
8) Confidence 0.62 Published 2010 Journal Respir Res Section Body Doc Link PMC2894769 Disease Relevance 0.94 Pain Relevance 0.36
In these same samples, LXA4 levels were highest in the mild asthma group[20,21].
Gene_expression (levels) of LXA4 associated with asthma
9) Confidence 0.62 Published 2010 Journal Respir Res Section Body Doc Link PMC2894769 Disease Relevance 1.39 Pain Relevance 0
In addition, LTB4/LXA4 ratios after LPS and dexamethasone were significantly greater in severe asthmatics compared to non-severe asthmatics (p < 0.05) as a result of both an increase in LTB4 and a decrease in LXA4 compared to normal subjects.


Gene_expression (ratios) of LXA4 associated with occupational lung diseases and dexamethasone
10) Confidence 0.62 Published 2010 Journal Respir Res Section Body Doc Link PMC2894769 Disease Relevance 1.18 Pain Relevance 0.34
There was a negative correlation between baseline LXA4 levels in asthmatic patients and the percentage of neutrophils in the BAL (rs = - 0.42, p < 0.05), and a positive correlation between LPS-induced LXA4 levels from asthmatic patients and FEV1 (% predicted; r = 0.60, p < 0.01).
Gene_expression (levels) of LXA4 in neutrophils associated with asthma
11) Confidence 0.62 Published 2010 Journal Respir Res Section Body Doc Link PMC2894769 Disease Relevance 1.04 Pain Relevance 0.03
The LPS induced formation of LTB4 was higher in severe asthma compared to non-severe asthma and normal subjects, while the LPS induced production of LXA4 was significantly impaired in severe asthmatics compared to normal subjects, but to a similar extent as in non-severe asthma patients.
Gene_expression (production) of LXA4 associated with asthma and occupational lung diseases
12) Confidence 0.55 Published 2010 Journal Respir Res Section Body Doc Link PMC2894769 Disease Relevance 1.45 Pain Relevance 0.26
In conjunction with the large number of alveolar macrophages in healthy and asthmatic lung, these observations provide support to the idea that the alveolar macrophage is a likely important source of LXA4 in human airways.
Gene_expression (source) of LXA4 in alveolar macrophages associated with asthma
13) Confidence 0.55 Published 2010 Journal Respir Res Section Body Doc Link PMC2894769 Disease Relevance 0.89 Pain Relevance 0
We measured leukotriene B4 (LTB4), and lipoxin A4 (LXA4) production by alveolar macrophages (AMs) and studied the impact of corticosteroids.


Gene_expression (production) of LXA4 in AMs associated with corticosteroid
14) Confidence 0.55 Published 2010 Journal Respir Res Section Abstract Doc Link PMC2894769 Disease Relevance 0.64 Pain Relevance 0.17
Together with the augmented LPS induced formation of LTB4 and decreased generation of LXA4 in severe asthma, our observations indicate a net pro-inflammatory imbalance in severe asthma.


Gene_expression (generation) of LXA4 associated with asthma and inflammation
15) Confidence 0.55 Published 2010 Journal Respir Res Section Body Doc Link PMC2894769 Disease Relevance 1.15 Pain Relevance 0.38
Although the levels of LXA4 are low, they were detected reproducibly, validated with authentic material and picogram quantities of LXs are biologically active in resolving inflammation (reviewed in reference [17]).
Gene_expression (levels) of LXA4 associated with inflammation
16) Confidence 0.55 Published 2010 Journal Respir Res Section Body Doc Link PMC2894769 Disease Relevance 0.87 Pain Relevance 0.39
Generation of LXA4 can decrease and LTB4 increase with age [41,42], but there is no information available at present on the influence of age on the release of these eicosanoids from human alveolar macrophages.
Gene_expression (Generation) of LXA4 in alveolar macrophages
17) Confidence 0.55 Published 2010 Journal Respir Res Section Body Doc Link PMC2894769 Disease Relevance 1.13 Pain Relevance 0.28
Thus, although the basal and stimulated levels of LXA4 from alveolar macrophages are in low picogram amounts, these levels would be predicted to have pro-resolving actions for airway inflammation (reviewed in [17].
Gene_expression (levels) of LXA4 in alveolar macrophages associated with inflammation
18) Confidence 0.55 Published 2010 Journal Respir Res Section Body Doc Link PMC2894769 Disease Relevance 1.01 Pain Relevance 0.45
Baseline and LPS-stimulated generation of LXA4
Gene_expression (generation) of LXA4
19) Confidence 0.55 Published 2010 Journal Respir Res Section Body Doc Link PMC2894769 Disease Relevance 0.83 Pain Relevance 0.08
We measured leukotriene B4 (LTB4), and lipoxin A4 (LXA4) production by alveolar macrophages (AMs) and studied the impact of corticosteroids.


Gene_expression (production) of lipoxin A4 in AMs associated with corticosteroid
20) Confidence 0.55 Published 2010 Journal Respir Res Section Abstract Doc Link PMC2894769 Disease Relevance 0.64 Pain Relevance 0.17

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