INT54358

Context Info Confidence 0.34 First Reported 1993 Last Reported 2008 Negated 0 Speculated 0 Reported most in Body Documents 13 Total Number 13 Disease Relevance 14.31 Pain Relevance 2.60

signal transduction (Ltb4r1) plasma membrane (Ltb4r1) signal transducer activity (Ltb4r1)

Anatomy Link Frequency PMNs 1 epithelium 1 lung 1 Ltb4r1 (Mus musculus)

Pain Link Frequency Relevance Heat Inflammatory mediators 65 100.00 Inflammation 268 99.40 Dynorphin 3 97.92 Morphine 6 96.34 Inflammatory response 68 95.44 narcan 5 86.32 Opioid 2 75.00 Enkephalin 3 69.08 opioid receptor 1 63.00 antagonist 6 61.40

Disease Link Frequency Relevance Heat INFLAMMATION 407 100.00 Pulmonary Disease 965 99.90 Pancreatic Cancer 84 97.98 Apoptosis 40 94.84 Nicotine Addiction 181 94.44 Cancer 144 88.32 Infection 9 88.24 Immunotherapy Of Cancer 2 66.80 Pneumonia 12 62.00 Asthma 31 59.52

Sentences Mentioned In

Key:

Protein

Mutation

Event

Anatomy

Negation

Speculation

Pain term

Disease term

Measurement of exhaled LTB4

Localization (Measurement) of LTB4

1) Confidence 0.34 Published 2005 Journal Respir Res Section Body Doc Link PMC1283153 Disease Relevance 0.06 Pain Relevance 0

The anti-pancreatic cancer activity of this extract is probably mediated through inhibition of LOX activity, since it inhibits LTB4 secretion.

Localization (secretion) of LTB4 associated with pancreatic cancer

2) Confidence 0.07 Published 2003 Journal Mol Cancer Section Body Doc Link PMC149414 Disease Relevance 1.03 Pain Relevance 0

Morphine was found to inhibit PMNs aggregation induced by PHA (0.01), PMA (0.01), fMLP (0.01) and Ca++ ionophore (p < 0.01), ATP release (p < 0.01), thromboxane B2 (TxB2) and leukotriene B4 (LTB4) secretion during cell aggregation.

Localization (secretion) of LTB4 in PMNs associated with morphine

3) Confidence 0.06 Published 1993 Journal Riv Eur Sci Med Farmacol Section Abstract Doc Link 7909619 Disease Relevance 0 Pain Relevance 1.24

ability of LTB4 to activate PPAR?

Localization (ability) of LTB4

4) Confidence 0.06 Published 2008 Journal PPAR Research Section Body Doc Link PMC2490577 Disease Relevance 1.01 Pain Relevance 0.47

Untreated COPD and non-COPD BES released the same levels of IL-8, PGE2 and LTB4 (Fig. 5A,B,C).

Localization (released) of LTB4 associated with pulmonary disease

5) Confidence 0.05 Published 2007 Journal Respir Res Section Body Doc Link PMC2214730 Disease Relevance 1.72 Pain Relevance 0

Also, LPS-induced release of IL-8 and PGE2 from COPD and non-COPD BES increased progressively overtime and peaked by 24 h, whereas LTB4 release increased up to 4 h and remained constant thereafter (Fig. 4D,E,F).

Localization (release) of LTB4 associated with pulmonary disease

6) Confidence 0.05 Published 2007 Journal Respir Res Section Body Doc Link PMC2214730 Disease Relevance 1.68 Pain Relevance 0.03

BES released the inflammatory mediators IL-8, PGE2 and LTB4 constitutively and following exposure to LPS.

Localization (released) of LTB4 associated with inflammatory mediators

7) Confidence 0.05 Published 2007 Journal Respir Res Section Abstract Doc Link PMC2214730 Disease Relevance 1.01 Pain Relevance 0.21

To our knowledge no previous studies have analyzed basal or LPS-induced PGE2 and LTB4 release by bronchial epithelium in COPD.

Localization (release) of LTB4 in epithelium associated with pulmonary disease

8) Confidence 0.05 Published 2007 Journal Respir Res Section Body Doc Link PMC2214730 Disease Relevance 1.37 Pain Relevance 0.14

No correlation was established between post bronchodilator FEV1 and PGE2 or LTB4 release (Fig. 5G,H,I).

Localization (release) of LTB4

9) Confidence 0.04 Published 2007 Journal Respir Res Section Body Doc Link PMC2214730 Disease Relevance 1.49 Pain Relevance 0

g/mL for 24 h), there was a 3-fold increase of IL-8 in COPD BES by comparison to non-COPD BES (Fig. 5D), whereas LPS-induced PGE2 and LTB4 release were similar in both COPD and non-COPD BES (Fig. 5E,F).

Localization (release) of LTB4 associated with pulmonary disease

10) Confidence 0.04 Published 2007 Journal Respir Res Section Body Doc Link PMC2214730 Disease Relevance 1.70 Pain Relevance 0

No correlation was observed between basal and LPS-induced release of PGE2 and LTB4 by BES and clinical and functional parameters of COPD and non-COPD patients (data not shown).

Localization (release) of LTB4 associated with pulmonary disease

11) Confidence 0.04 Published 2007 Journal Respir Res Section Body Doc Link PMC2214730 Disease Relevance 0.81 Pain Relevance 0.04

In our study, we chose to stimulate BES with lipopolycaccharide (LPS) and measured the release of the pro-inflammatory mediators interleukin-8 (IL-8) and leukotriene B4 (LTB4) and the anti-inflammatory mediator prostaglandin E2 (PGE2).

Localization (release) of LTB4 associated with inflammatory mediators and inflammation

12) Confidence 0.04 Published 2007 Journal Respir Res Section Abstract Doc Link PMC2214730 Disease Relevance 1.44 Pain Relevance 0.28

Interestingly, LPS induced a higher release of IL-8, but not PGE2 and LTB4 in COPD BES (p < 0.001) which correlated with lung function changes.

Localization (release) of LTB4 in lung associated with pulmonary disease

13) Confidence 0.02 Published 2007 Journal Respir Res Section Abstract Doc Link PMC2214730 Disease Relevance 0.96 Pain Relevance 0.19

General Comments

This test has worked.