| pubmed-article:18354232 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18354232 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:18354232 | lifeskim:mentions | umls-concept:C0026473 | lld:lifeskim |
| pubmed-article:18354232 | lifeskim:mentions | umls-concept:C0033618 | lld:lifeskim |
| pubmed-article:18354232 | lifeskim:mentions | umls-concept:C0023810 | lld:lifeskim |
| pubmed-article:18354232 | lifeskim:mentions | umls-concept:C1367477 | lld:lifeskim |
| pubmed-article:18354232 | lifeskim:mentions | umls-concept:C1333908 | lld:lifeskim |
| pubmed-article:18354232 | lifeskim:mentions | umls-concept:C1819464 | lld:lifeskim |
| pubmed-article:18354232 | lifeskim:mentions | umls-concept:C1705822 | lld:lifeskim |
| pubmed-article:18354232 | lifeskim:mentions | umls-concept:C0348011 | lld:lifeskim |
| pubmed-article:18354232 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
| pubmed-article:18354232 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:18354232 | pubmed:dateCreated | 2008-3-20 | lld:pubmed |
| pubmed-article:18354232 | pubmed:abstractText | LPS-binding protein (LBP) is a central mediator that transfers LPS to CD14 to initiate TLR4-mediated proinflammatory response. However, a possibility of another LPS transfer molecule has been suggested because LBP-deficient mice showed almost normal inflammatory response after LPS injection. In this study, we describe the novel finding that high mobility group box 1 protein (HMGB1) recently identified as a mediator of sepsis has a function of LPS transfer for a proinflammatory response. We used ELISA and surface plasmon resonance to show that HMGB1 binds LPS in a concentration-dependent manner and that the binding is stronger to lipid A moiety than to the polysaccharide moiety of LPS. This binding was inhibited by LBP and polymyxin B. Using native PAGE and fluorescence-based LPS transfer analyses, we show that HMGB1 can catalytically disaggregate and transfer LPS to both soluble CD14 protein and to human PBMCs in a dose-dependent manner. However, this effect was dramatically reduced to the baseline level when HMGB1 was heat inactivated. Furthermore, a mixture of HMGB1 and LPS treatment results in a higher increase in TNF-alpha production in human PBMCs and peripheral blood monocytes than LPS or HMGB1 treatment alone or their summation. Thus, we propose that HMGB1 plays an important role in Gram-negative sepsis by catalyzing movement of LPS monomers from LPS aggregates to CD14 to initiate a TLR4-mediated proinflammatory response. | lld:pubmed |
| pubmed-article:18354232 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18354232 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18354232 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:18354232 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18354232 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18354232 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18354232 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18354232 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18354232 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18354232 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:18354232 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:18354232 | pubmed:author | pubmed-author:ShinJeon-SooJ... | lld:pubmed |
| pubmed-article:18354232 | pubmed:author | pubmed-author:KimEun SookES | lld:pubmed |
| pubmed-article:18354232 | pubmed:author | pubmed-author:YounJu HoJH | lld:pubmed |
| pubmed-article:18354232 | pubmed:author | pubmed-author:ChoiJi EunJE | lld:pubmed |
| pubmed-article:18354232 | pubmed:author | pubmed-author:OhYoung JooYJ | lld:pubmed |
| pubmed-article:18354232 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:18354232 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:18354232 | pubmed:volume | 180 | lld:pubmed |
| pubmed-article:18354232 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18354232 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18354232 | pubmed:pagination | 5067-74 | lld:pubmed |
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| pubmed-article:18354232 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18354232 | pubmed:articleTitle | High mobility group box 1 protein binding to lipopolysaccharide facilitates transfer of lipopolysaccharide to CD14 and enhances lipopolysaccharide-mediated TNF-alpha production in human monocytes. | lld:pubmed |
| pubmed-article:18354232 | pubmed:affiliation | Department of Microbiology, Brain Korea 21 Project for Medical Science, National Core Research Center for Nanomedical Technology, Yonsei University College of Medicine, Seoul, Republic of Korea. | lld:pubmed |
| pubmed-article:18354232 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18354232 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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