pubmed-article:2651523 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:2651523 | lifeskim:mentions | umls-concept:C0021755 | lld:lifeskim |
pubmed-article:2651523 | lifeskim:mentions | umls-concept:C0023810 | lld:lifeskim |
pubmed-article:2651523 | lifeskim:mentions | umls-concept:C0678594 | lld:lifeskim |
pubmed-article:2651523 | lifeskim:mentions | umls-concept:C0728938 | lld:lifeskim |
pubmed-article:2651523 | lifeskim:mentions | umls-concept:C1704788 | lld:lifeskim |
pubmed-article:2651523 | pubmed:issue | 9 | lld:pubmed |
pubmed-article:2651523 | pubmed:dateCreated | 1989-5-31 | lld:pubmed |
pubmed-article:2651523 | pubmed:abstractText | Natural and synthetic lipid A as well as natural and synthetic oligosaccharide partial structures of LPS were examined in dose-response experiments to define the minimal structure necessary for IL-1 induction and release in cultures of human mononuclear cells. Wild type LPS (S. abortus equi) and rough mutant LPS was active in minimal-doses of 1 to 100 pg/ml, whereas synthetic heptaacyl and hexaacyl lipid A (Salmonella minnesota and Escherichia coli lipid A, respectively) induced IL-1 in minimal-doses of 100 to 1,000 pg/ml and 10 to 1,000 pg/ml, respectively. Nanogram amounts (0.1 to 10 ng/ml) of synthetic monodephospho partial structures of E. coli lipid A were necessary for IL-1 induction. Synthetic pentaacyl partial structures induced IL-1 very weakly. Synthetic tetraacyl and bisacyl partial structures lacking non-hydroxylated fatty acids were not active. Compared to LPS million-fold higher doses of natural and synthetic 3-deoxy-D-manno-octulosonic acid containing core oligosaccharides were necessary for IL-1 induction. Dose-response investigations with LPS and natural or synthetic partial structures established the following hierarchy in IL-1 induction-capacity: LPS greater than lipid A much greater than lipid A partial structures greater than core oligosaccharides greater than oligoacyl lipid A. Lipid A was shown here to be the portion of LPS mainly responsible for induction of IL-1 activity. The high potency of lipid A in inducing IL-1 release and the failure of the precursor Ia of lipid A to induce IL-1 production and release was also observed measuring intracellular IL-1 activity after freeze-thawing the cells. Levels of IL-1 beta mRNA in extracts of mononuclear cells correlated with biologic activity. In co-incubation experiments, precursor Ia of lipid A produced dose-dependent inhibition of production and release of IL-1 activity induced by lipid A or LPS, but not by Staphylococcus epidermidis or PHA. Incubation of cells with precursor Ia for 1h, followed by a medium change and further incubation of stimulus without precursor Ia of lipid A also resulted in inhibition. We conclude that lipid A is the main portion of LPS responsible for induction of IL-1, and that specific activation- and/or binding-mechanisms are involved in stimulation of cells with LPS and/or lipid A. | lld:pubmed |
pubmed-article:2651523 | pubmed:language | eng | lld:pubmed |
pubmed-article:2651523 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2651523 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:2651523 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:2651523 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2651523 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:2651523 | pubmed:month | May | lld:pubmed |
pubmed-article:2651523 | pubmed:issn | 0022-1767 | lld:pubmed |
pubmed-article:2651523 | pubmed:author | pubmed-author:GATEM AMA | lld:pubmed |
pubmed-article:2651523 | pubmed:author | pubmed-author:DinarelloC... | lld:pubmed |
pubmed-article:2651523 | pubmed:author | pubmed-author:KusumotoSS | lld:pubmed |
pubmed-article:2651523 | pubmed:author | pubmed-author:RietschelE... | lld:pubmed |
pubmed-article:2651523 | pubmed:author | pubmed-author:BradeHH | lld:pubmed |
pubmed-article:2651523 | pubmed:author | pubmed-author:LoppnowHH | lld:pubmed |
pubmed-article:2651523 | pubmed:author | pubmed-author:DürrbaumII | lld:pubmed |
pubmed-article:2651523 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:2651523 | pubmed:day | 1 | lld:pubmed |
pubmed-article:2651523 | pubmed:volume | 142 | lld:pubmed |
pubmed-article:2651523 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:2651523 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:2651523 | pubmed:pagination | 3229-38 | lld:pubmed |
pubmed-article:2651523 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:2651523 | pubmed:meshHeading | pubmed-meshheading:2651523-... | lld:pubmed |
pubmed-article:2651523 | pubmed:year | 1989 | lld:pubmed |
pubmed-article:2651523 | pubmed:articleTitle | IL-1 induction-capacity of defined lipopolysaccharide partial structures. | lld:pubmed |
pubmed-article:2651523 | pubmed:affiliation | Department of Immunologie, Forschungsinstitut Borstel, FRG. | lld:pubmed |
pubmed-article:2651523 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:2651523 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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