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rdf:type |
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lifeskim:mentions |
umls-concept:C0027950,
umls-concept:C0031090,
umls-concept:C0048893,
umls-concept:C0182953,
umls-concept:C0205314,
umls-concept:C0333516,
umls-concept:C0599896,
umls-concept:C0620604,
umls-concept:C0679622,
umls-concept:C0871261,
umls-concept:C1522496,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C2347946,
umls-concept:C2911692
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pubmed:issue |
7
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pubmed:dateCreated |
2000-3-23
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pubmed:abstractText |
The impact of lipoxin A4 (LXA4) and aspirin-triggered-lipoxins (ATL) was investigated in tumor necrosis factor (TNF alpha)-initiated neutrophil (PMN) responses in vitro and in vivo using LX analogs that are metabolically more stable. At nanomolar levels, the LXA4 and ATL analog 15 R/S-methyl-LXA4 each blocked TNF alpha-stimulated IL-1 beta release by isolated human PMN in vitro. These LXA4-ATL actions were time- and concentration-dependent. The TNF alpha-induced IL-1 beta gene expression was also regulated by 15 R/S-methyl-LXA4. In addition, 15 R/S-methyl-LXA4 added to murine air pouches dramatically inhibited TNF alpha-stimulated leukocyte trafficking in vivo, as well as altered the appearance of both macrophage inflammatory peptide-2 and IL-1 beta and concomitantly stimulated IL-4 in pouch exudates. These findings from in vitro and in vivo experiments indicate that both LXA4 and ATL are regulators of TNF alpha-directed neutrophil actions and stimulate IL-4 in exudates and thus regulate mediators that are held to play an important role in the pathogenesis of periodontal disease.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
D
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Inflammatory Agents...,
http://linkedlifedata.com/resource/pubmed/chemical/Aspirin,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL2,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines,
http://linkedlifedata.com/resource/pubmed/chemical/Chemotactic Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Hydroxyeicosatetraenoic Acids,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/Lipoxins,
http://linkedlifedata.com/resource/pubmed/chemical/Monokines,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/lipoxin A4
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0022-3484
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
34
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
370-3
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:10685363-Animals,
pubmed-meshheading:10685363-Anti-Inflammatory Agents, Non-Steroidal,
pubmed-meshheading:10685363-Aspirin,
pubmed-meshheading:10685363-Chemokine CXCL2,
pubmed-meshheading:10685363-Chemokines,
pubmed-meshheading:10685363-Chemotactic Factors,
pubmed-meshheading:10685363-Cytokines,
pubmed-meshheading:10685363-Dose-Response Relationship, Drug,
pubmed-meshheading:10685363-Gene Expression Regulation,
pubmed-meshheading:10685363-Humans,
pubmed-meshheading:10685363-Hydroxyeicosatetraenoic Acids,
pubmed-meshheading:10685363-Interleukin-1,
pubmed-meshheading:10685363-Interleukin-4,
pubmed-meshheading:10685363-Lipoxins,
pubmed-meshheading:10685363-Male,
pubmed-meshheading:10685363-Mice,
pubmed-meshheading:10685363-Mice, Inbred BALB C,
pubmed-meshheading:10685363-Monokines,
pubmed-meshheading:10685363-Neutrophil Infiltration,
pubmed-meshheading:10685363-Neutrophils,
pubmed-meshheading:10685363-Periodontal Diseases,
pubmed-meshheading:10685363-Stereoisomerism,
pubmed-meshheading:10685363-Tumor Necrosis Factor-alpha
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pubmed:year |
1999
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pubmed:articleTitle |
Lipoxin A4 and aspirin-triggered 15-epi-LXA4 inhibit tumor necrosis factor-alpha-initiated neutrophil responses and trafficking: novel regulators of a cytokine-chemokine axis relevant to periodontal diseases.
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pubmed:affiliation |
Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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