| pubmed-article:20439476 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20439476 | lifeskim:mentions | umls-concept:C0027575 | lld:lifeskim |
| pubmed-article:20439476 | lifeskim:mentions | umls-concept:C0025303 | lld:lifeskim |
| pubmed-article:20439476 | lifeskim:mentions | umls-concept:C0023767 | lld:lifeskim |
| pubmed-article:20439476 | lifeskim:mentions | umls-concept:C1274040 | lld:lifeskim |
| pubmed-article:20439476 | lifeskim:mentions | umls-concept:C0678594 | lld:lifeskim |
| pubmed-article:20439476 | lifeskim:mentions | umls-concept:C1517004 | lld:lifeskim |
| pubmed-article:20439476 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:20439476 | pubmed:dateCreated | 2010-6-17 | lld:pubmed |
| pubmed-article:20439476 | pubmed:abstractText | Lipopolysaccharide (LPS), a major component of the meningococcal outer membrane, is sensed by the host through activation of Toll-like receptor 4 (TLR4). Recently, we demonstrated that a surprisingly large fraction of Neisseria meningitidis disease isolates are lipid A mutants, due to inactivating mutations in the lpxL1 gene. The lpxL1 mutants activate human TLR4 much less efficiently than wild-type bacteria, which may be advantageous by allowing them to escape from the innate immune system. Here we investigated the influence of lipid A structure on virulence in a mouse model of meningococcal sepsis. One limitation, however, is that murine TLR4 recognizes lpxL1 mutant bacteria much better than human TLR4. We show that an lpxL2 mutant, another lipid A mutant lacking an acyl chain at a different position, activates murine TLR4 less efficiently than the lpxL1 mutant. Therefore, the lpxL2 mutant in mice might be a better model for infections with lpxL1 mutants in humans. Interestingly, we found that the lpxL2 mutant is more virulent in mice than the wild-type strain, whereas the lpxL1 mutant is actually much less virulent than the wild-type strain. These results demonstrate the crucial role of N. meningitidis lipid A structure in virulence. | lld:pubmed |
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| pubmed-article:20439476 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20439476 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20439476 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:20439476 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20439476 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:20439476 | pubmed:issn | 1098-5522 | lld:pubmed |
| pubmed-article:20439476 | pubmed:author | pubmed-author:van der... | lld:pubmed |
| pubmed-article:20439476 | pubmed:author | pubmed-author:BoogClaire... | lld:pubmed |
| pubmed-article:20439476 | pubmed:author | pubmed-author:van... | lld:pubmed |
| pubmed-article:20439476 | pubmed:author | pubmed-author:van den... | lld:pubmed |
| pubmed-article:20439476 | pubmed:author | pubmed-author:HamstraHendri... | lld:pubmed |
| pubmed-article:20439476 | pubmed:author | pubmed-author:FransenFloris... | lld:pubmed |
| pubmed-article:20439476 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20439476 | pubmed:volume | 78 | lld:pubmed |
| pubmed-article:20439476 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20439476 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20439476 | pubmed:pagination | 3177-86 | lld:pubmed |
| pubmed-article:20439476 | pubmed:dateRevised | 2011-7-19 | lld:pubmed |
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