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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
1994-10-5
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pubmed:abstractText |
C3H/HeJ (Lpsd) macrophages have been shown to respond to certain LPSs, especially from rough mutant bacteria. C3H/OuJ (Lpsn) macrophages are induced by wild-type LPS, rough LPS, or lipid A to express many genes, including TNF-alpha, TNFR-2, IL-1 beta, IP-10, D3, and D8. C3H/HeJ macrophages failed to induce any of these genes when cultured with wild-type LPS or synthetic lipid A, even when pretreated with IFN-gamma. However, rough mutant Salmonella minnesota Ra, Rc, and Rd LPS, and Escherichia coli D31 m3 Rd LPS induced Lpsd macrophages to express a subset of genes within the gene panel. Because bioactive preparations contained trace quantities of endotoxin protein(s), a deoxycholate-modified, phenol-water method was used to repurify rough LPS into an aqueous phase, and extract endotoxin proteins into a phenol phase. Repurified LPS failed to stimulate Lpsd macrophages; however, phenol fractions were approximately 10% as potent in Lpsd macrophages as crude rough LPS. Full potency was restored in C3H/HeJ macrophages when aqueous phase LPS and phenol-phase proteins were co-precipitated, suggesting that LPS and endotoxin proteins interact synergistically. Endotoxin proteins alone induced TNF-alpha, TNFR-2, and IL-1 beta, but not IP-10, D3, and D8 genes in both Lpsd and Lpsn macrophages. Tyrosine phosphorylation of three 41- to 47-kDa proteins was induced by endotoxin proteins, but not by LPS, in Lpsd macrophages. Thus, endotoxin proteins seem to activate a signaling pathway(s) that converges (distal to the Lps gene product) with a subset of LPS-signaling pathways.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Endotoxins,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Lipid A,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphotyrosine,
http://linkedlifedata.com/resource/pubmed/chemical/Tyrosine
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
153
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pubmed:geneSymbol |
Lps
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2653-63
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:7521367-Animals,
pubmed-meshheading:7521367-Blotting, Northern,
pubmed-meshheading:7521367-Cells, Cultured,
pubmed-meshheading:7521367-Endotoxins,
pubmed-meshheading:7521367-Gene Expression Regulation,
pubmed-meshheading:7521367-Immunoblotting,
pubmed-meshheading:7521367-Interferon-gamma,
pubmed-meshheading:7521367-Lipid A,
pubmed-meshheading:7521367-Lipopolysaccharides,
pubmed-meshheading:7521367-Macrophages,
pubmed-meshheading:7521367-Mice,
pubmed-meshheading:7521367-Mice, Inbred C3H,
pubmed-meshheading:7521367-Phosphotyrosine,
pubmed-meshheading:7521367-Tyrosine
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pubmed:year |
1994
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pubmed:articleTitle |
Endotoxin-induced early gene expression in C3H/HeJ (Lpsd) macrophages.
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pubmed:affiliation |
Department of Microbiology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.
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