pubmed-article:8973571 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8973571 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:8973571 | lifeskim:mentions | umls-concept:C0125090 | lld:lifeskim |
pubmed-article:8973571 | lifeskim:mentions | umls-concept:C0027950 | lld:lifeskim |
pubmed-article:8973571 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:8973571 | pubmed:dateCreated | 1997-1-27 | lld:pubmed |
pubmed-article:8973571 | pubmed:abstractText | The activation of leucocytes by bacterial cell wall lipopolysaccharide (LPS) contributes to the pathogenesis of septic shock. LPS is known to interact with several cell-surface proteins, including CD14, when presented as a complex with serum LPS-binding protein. However, the identity of the receptor responsible for LPS signalling and leucocyte activation is unknown. Interestingly, mice deficient in cell-surface L-selectin were dramatically resistant to the lethal effects of high doses of LPS in a model of septic shock. Recently we reported that L-selectin binds to cardiolipin and other charged phospholipids at a site distinct from the carbohydrate-binding site. Structural similarities between charged phospholipids and the lipid A moiety of LPS prompted us to investigate interactions between L-selectin and LPS. Herein we show that L-selectin is a neutrophil surface receptor for LPS and lipotechoic acid. The binding of LPS to L-selectin is independent of serum and Ca2+, and is blocked by antibodies to L-selectin and fucoidan. Furthermore, the interaction of LPS with cell-surface L-selectin results in superoxide production, indicating that L-selectin can mediate both binding and activation of human neutrophils. These findings suggest novel therapeutic approaches for the treatment of septic shock. | lld:pubmed |
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pubmed-article:8973571 | pubmed:language | eng | lld:pubmed |
pubmed-article:8973571 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8973571 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:8973571 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8973571 | pubmed:month | Dec | lld:pubmed |
pubmed-article:8973571 | pubmed:issn | 0264-6021 | lld:pubmed |
pubmed-article:8973571 | pubmed:author | pubmed-author:BirdM IMI | lld:pubmed |
pubmed-article:8973571 | pubmed:author | pubmed-author:MalhotraRR | lld:pubmed |
pubmed-article:8973571 | pubmed:author | pubmed-author:PriestRR | lld:pubmed |
pubmed-article:8973571 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8973571 | pubmed:day | 1 | lld:pubmed |
pubmed-article:8973571 | pubmed:volume | 320 ( Pt 2) | lld:pubmed |
pubmed-article:8973571 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8973571 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8973571 | pubmed:pagination | 589-93 | lld:pubmed |
pubmed-article:8973571 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:8973571 | pubmed:year | 1996 | lld:pubmed |
pubmed-article:8973571 | pubmed:articleTitle | Role for L-selectin in lipopolysaccharide-induced activation of neutrophils. | lld:pubmed |
pubmed-article:8973571 | pubmed:affiliation | Glycobiology Research Unit, Glaxo Wellcome Medicines Research Centre, Stevenage, Herts, 2NY, U.K. | lld:pubmed |
pubmed-article:8973571 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:8973571 | pubmed:publicationType | Comparative Study | lld:pubmed |
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