| pubmed-article:1730468 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1730468 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:1730468 | lifeskim:mentions | umls-concept:C0043409 | lld:lifeskim |
| pubmed-article:1730468 | lifeskim:mentions | umls-concept:C0032176 | lld:lifeskim |
| pubmed-article:1730468 | lifeskim:mentions | umls-concept:C0127400 | lld:lifeskim |
| pubmed-article:1730468 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:1730468 | pubmed:dateCreated | 1992-2-18 | lld:pubmed |
| pubmed-article:1730468 | pubmed:abstractText | Plasmid-free strains of Yersinia pseudotuberculosis induce aggregation of human platelets in vitro. It appears that this phenomenon is mediated by invasin (Inv), a 103-kDa outer membrane protein that permits bacteria to penetrate mammalian cells, since (i) an isogenic inv-deficient mutant failed to aggregate platelets compared with the parental strain; (ii) a monoclonal antibody directed against invasin inhibited platelet aggregation; (iii) Inv+ Escherichia coli HB101 promoted platelet aggregation. Platelet receptors for invasin were identified by using a panel of anti-platelet glycoprotein monoclonal antibodies in a bacterial adhesion assay. We found that bacteria bind to platelet membrane glycoproteins Ic and IIa. Electron microscopic study of bacterium-platelet interactions also revealed that bacteria expressing invasin attach to and are phagocytized by thrombocytes, in contrast to inv-deficient bacteria, indicating that these anucleated cells are able to internalize bacteria in vitro after specific interaction with invasin. | lld:pubmed |
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| pubmed-article:1730468 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:1730468 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1730468 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1730468 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:1730468 | pubmed:issn | 0019-9567 | lld:pubmed |
| pubmed-article:1730468 | pubmed:author | pubmed-author:KaplanCC | lld:pubmed |
| pubmed-article:1730468 | pubmed:author | pubmed-author:BerchePP | lld:pubmed |
| pubmed-article:1730468 | pubmed:author | pubmed-author:FrehelCC | lld:pubmed |
| pubmed-article:1730468 | pubmed:author | pubmed-author:SimonetMM | lld:pubmed |
| pubmed-article:1730468 | pubmed:author | pubmed-author:Morel-KoppM... | lld:pubmed |
| pubmed-article:1730468 | pubmed:author | pubmed-author:TriadouPP | lld:pubmed |
| pubmed-article:1730468 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1730468 | pubmed:volume | 60 | lld:pubmed |
| pubmed-article:1730468 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1730468 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1730468 | pubmed:pagination | 366-73 | lld:pubmed |
| pubmed-article:1730468 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:1730468 | pubmed:meshHeading | pubmed-meshheading:1730468-... | lld:pubmed |
| pubmed-article:1730468 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1730468 | pubmed:articleTitle | Human platelet aggregation by Yersinia pseudotuberculosis is mediated by invasin. | lld:pubmed |
| pubmed-article:1730468 | pubmed:affiliation | Laboratoire de Microbiologie, Faculté de Médecine Necker-Enfants Malades, Paris, France. | lld:pubmed |
| pubmed-article:1730468 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1730468 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:1730468 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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