| pubmed-article:10685363 | rdf:type | pubmed:Citation | lld:pubmed |
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| pubmed-article:10685363 | lifeskim:mentions | umls-concept:C0027950 | lld:lifeskim |
| pubmed-article:10685363 | lifeskim:mentions | umls-concept:C1522496 | lld:lifeskim |
| pubmed-article:10685363 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
| pubmed-article:10685363 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
| pubmed-article:10685363 | lifeskim:mentions | umls-concept:C0333516 | lld:lifeskim |
| pubmed-article:10685363 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
| pubmed-article:10685363 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
| pubmed-article:10685363 | lifeskim:mentions | umls-concept:C0599896 | lld:lifeskim |
| pubmed-article:10685363 | lifeskim:mentions | umls-concept:C0182953 | lld:lifeskim |
| pubmed-article:10685363 | lifeskim:mentions | umls-concept:C0679622 | lld:lifeskim |
| pubmed-article:10685363 | lifeskim:mentions | umls-concept:C0205314 | lld:lifeskim |
| pubmed-article:10685363 | lifeskim:mentions | umls-concept:C2347946 | lld:lifeskim |
| pubmed-article:10685363 | lifeskim:mentions | umls-concept:C0048893 | lld:lifeskim |
| pubmed-article:10685363 | lifeskim:mentions | umls-concept:C0620604 | lld:lifeskim |
| pubmed-article:10685363 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:10685363 | pubmed:dateCreated | 2000-3-23 | lld:pubmed |
| pubmed-article:10685363 | 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. | lld:pubmed |
| pubmed-article:10685363 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10685363 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10685363 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10685363 | pubmed:citationSubset | D | lld:pubmed |
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| pubmed-article:10685363 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10685363 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:10685363 | pubmed:issn | 0022-3484 | lld:pubmed |
| pubmed-article:10685363 | pubmed:author | pubmed-author:PouliotMM | lld:pubmed |
| pubmed-article:10685363 | pubmed:author | pubmed-author:SerhanC NCN | lld:pubmed |
| pubmed-article:10685363 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10685363 | pubmed:volume | 34 | lld:pubmed |
| pubmed-article:10685363 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10685363 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10685363 | pubmed:pagination | 370-3 | lld:pubmed |
| pubmed-article:10685363 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:10685363 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10685363 | 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. | lld:pubmed |
| pubmed-article:10685363 | pubmed:affiliation | Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. | lld:pubmed |
| pubmed-article:10685363 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10685363 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:10685363 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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