| pubmed-article:2731990 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2731990 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:2731990 | lifeskim:mentions | umls-concept:C0023820 | lld:lifeskim |
| pubmed-article:2731990 | lifeskim:mentions | umls-concept:C0026473 | lld:lifeskim |
| pubmed-article:2731990 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:2731990 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:2731990 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:2731990 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:2731990 | pubmed:dateCreated | 1989-7-18 | lld:pubmed |
| pubmed-article:2731990 | pubmed:abstractText | Toxicity of lipopolysaccharide (LPS) (endotoxin) is, to a large extent, mediated by the activation of monocytes/macrophages and subsequent release of monokines, such as interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-alpha). It is known that LPS binds readily to serum lipoproteins and that LPS-lipoprotein complexes are less toxic than unbound LPS. Here we present data analyzing the impact of the LPS-serum interaction at the cellular level. By measuring IL-1 TNF-alpha, and IL-6, the interaction of different LPSs or lipid A with human serum could be shown to prevent the activation of human monocytes. The amounts of LPS inactivated by normal human serum did not exceed 10 ng/ml. The LPS-inactivating capacity of serum was shown to be a function of the lipoproteins. Other serum components, such as naturally occurring anti-LPS immunoglobulin G, complement, or nutritive lipids, had no significant influence in our system. Our experiments suggest that serum lipoproteins control endotoxin-induced monocyte activation and monokine release. | lld:pubmed |
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| pubmed-article:2731990 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2731990 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2731990 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:2731990 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2731990 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:2731990 | pubmed:issn | 0019-9567 | lld:pubmed |
| pubmed-article:2731990 | pubmed:author | pubmed-author:NorthoffHH | lld:pubmed |
| pubmed-article:2731990 | pubmed:author | pubmed-author:MännelD NDN | lld:pubmed |
| pubmed-article:2731990 | pubmed:author | pubmed-author:FlegelW AWA | lld:pubmed |
| pubmed-article:2731990 | pubmed:author | pubmed-author:WölplAA | lld:pubmed |
| pubmed-article:2731990 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2731990 | pubmed:volume | 57 | lld:pubmed |
| pubmed-article:2731990 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2731990 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2731990 | pubmed:pagination | 2237-45 | lld:pubmed |
| pubmed-article:2731990 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:2731990 | pubmed:year | 1989 | lld:pubmed |
| pubmed-article:2731990 | pubmed:articleTitle | Inhibition of endotoxin-induced activation of human monocytes by human lipoproteins. | lld:pubmed |
| pubmed-article:2731990 | pubmed:affiliation | DRK-Blutspendezentrale, Universität Ulm, Federal Republic of Germany. | lld:pubmed |
| pubmed-article:2731990 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2731990 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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