| pubmed-article:12952922 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12952922 | lifeskim:mentions | umls-concept:C0025289 | lld:lifeskim |
| pubmed-article:12952922 | lifeskim:mentions | umls-concept:C0038402 | lld:lifeskim |
| pubmed-article:12952922 | lifeskim:mentions | umls-concept:C0348801 | lld:lifeskim |
| pubmed-article:12952922 | lifeskim:mentions | umls-concept:C0014257 | lld:lifeskim |
| pubmed-article:12952922 | lifeskim:mentions | umls-concept:C0027950 | lld:lifeskim |
| pubmed-article:12952922 | lifeskim:mentions | umls-concept:C0006104 | lld:lifeskim |
| pubmed-article:12952922 | lifeskim:mentions | umls-concept:C0070410 | lld:lifeskim |
| pubmed-article:12952922 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
| pubmed-article:12952922 | lifeskim:mentions | umls-concept:C0086982 | lld:lifeskim |
| pubmed-article:12952922 | lifeskim:mentions | umls-concept:C1515877 | lld:lifeskim |
| pubmed-article:12952922 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:12952922 | lifeskim:mentions | umls-concept:C1880177 | lld:lifeskim |
| pubmed-article:12952922 | lifeskim:mentions | umls-concept:C0441836 | lld:lifeskim |
| pubmed-article:12952922 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:12952922 | pubmed:dateCreated | 2003-9-3 | lld:pubmed |
| pubmed-article:12952922 | pubmed:abstractText | Meningitis occurs when blood-borne pathogens cross the blood-brain barrier (BBB) in a complex interplay between endothelial cells and microbial gene products. We sought to understand the initial response of the BBB to the human meningeal pathogen group B Streptococcus (GBS) and the organism's major virulence factors, the exopolysaccharide capsule and the beta-hemolysin/cytolysin toxin (beta-h/c). Using oligonucleotide microarrays, we found that GBS infection of human brain microvascular endothelial cells (HBMEC) induced a highly specific and coordinate set of genes including IL-8, Groalpha, Grobeta, IL-6, GM-CSF, myeloid cell leukemia sequence-1 (Mcl-1), and ICAM-1, which act to orchestrate neutrophil recruitment, activation, and enhanced survival. Most strikingly, infection with a GBS strain lacking beta-h/c resulted in a marked reduction in expression of genes involved in the immune response, while the unencapsulated strain generally induced similar or greater expression levels for the same subset of genes. Cell-free bacterial supernatants containing beta-h/c activity induced IL-8 release, identifying this toxin as a principal provocative factor for BBB activation. These findings were further substantiated in vitro and in vivo. Neutrophil migration across polar HBMEC monolayers was stimulated by GBS and its beta-h/c through a process involving IL-8 and ICAM-1. In a murine model of hematogenous meningitis, mice infected with beta-h/c mutants exhibited lower mortality and decreased brain bacterial counts compared with mice infected with the corresponding WT GBS strains. | lld:pubmed |
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| pubmed-article:12952922 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12952922 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12952922 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:12952922 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12952922 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:12952922 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:12952922 | pubmed:author | pubmed-author:NizetVictorV | lld:pubmed |
| pubmed-article:12952922 | pubmed:author | pubmed-author:DoranKelly... | lld:pubmed |
| pubmed-article:12952922 | pubmed:author | pubmed-author:LiuGeorge YGY | lld:pubmed |
| pubmed-article:12952922 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12952922 | pubmed:volume | 112 | lld:pubmed |
| pubmed-article:12952922 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12952922 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12952922 | pubmed:pagination | 736-44 | lld:pubmed |
| pubmed-article:12952922 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:12952922 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12952922 | pubmed:articleTitle | Group B streptococcal beta-hemolysin/cytolysin activates neutrophil signaling pathways in brain endothelium and contributes to development of meningitis. | lld:pubmed |
| pubmed-article:12952922 | pubmed:affiliation | Department of Pediatrics, University of California, San Diego, School of Medicine, La Jolla, California 92093-0672, USA. kdoran@ucsd.edu | lld:pubmed |
| pubmed-article:12952922 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12952922 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:12952922 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:12952922 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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