| pubmed-article:3084560 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:3084560 | lifeskim:mentions | umls-concept:C0521009 | lld:lifeskim |
| pubmed-article:3084560 | lifeskim:mentions | umls-concept:C1819995 | lld:lifeskim |
| pubmed-article:3084560 | lifeskim:mentions | umls-concept:C0009498 | lld:lifeskim |
| pubmed-article:3084560 | lifeskim:mentions | umls-concept:C1261381 | lld:lifeskim |
| pubmed-article:3084560 | lifeskim:mentions | umls-concept:C0439859 | lld:lifeskim |
| pubmed-article:3084560 | lifeskim:mentions | umls-concept:C0065067 | lld:lifeskim |
| pubmed-article:3084560 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:3084560 | pubmed:dateCreated | 1986-6-3 | lld:pubmed |
| pubmed-article:3084560 | pubmed:abstractText | Lipoteichoic acids (LTA) released by gram-positive bacteria can spontaneously bind to mammalian cell surfaces. In the present study, erythrocytes (E) sensitized with pneumococcal LTA (LTA-E) were used as a model system to determine if LTA could render host cells susceptible to damage by autologous complement. Complement (C)-mediated lysis of LTA-E from normal rats and normal humans occurred when these cells were incubated in their respective autologous sera in vitro. In addition, when LTA-E from a C2-deficient human and from C4-deficient guinea pigs were incubated in their autologous sera, there was significant lysis in vitro, demonstrating a role for the alternative pathway. The in vivo survival of 51Cr-labeled autologous LTA-E was also studied. Only 2.9% of autologous LTA-E remained in the circulation of normal rats after 90 min. In contrast, 31.2% of autologous LTA-E remained in the circulation of rats depleted of C3. Intravascular hemolysis accounted for the clearance of LTA-E in the normal rats, whereas liver sequestration was responsible for clearance in the C3-depleted rats. These results demonstrate that LTA can render the host's cells susceptible to damage by its own complement system, establishing this as a possible mechanism of tissue damage in natural bacterial infections. | lld:pubmed |
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| pubmed-article:3084560 | pubmed:language | eng | lld:pubmed |
| pubmed-article:3084560 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3084560 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:3084560 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:3084560 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:3084560 | pubmed:month | May | lld:pubmed |
| pubmed-article:3084560 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:3084560 | pubmed:author | pubmed-author:WinkelsteinJ... | lld:pubmed |
| pubmed-article:3084560 | pubmed:author | pubmed-author:HummellD SDS | lld:pubmed |
| pubmed-article:3084560 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:3084560 | pubmed:volume | 77 | lld:pubmed |
| pubmed-article:3084560 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:3084560 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:3084560 | pubmed:pagination | 1533-8 | lld:pubmed |
| pubmed-article:3084560 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:3084560 | pubmed:year | 1986 | lld:pubmed |
| pubmed-article:3084560 | pubmed:articleTitle | Bacterial lipoteichoic acid sensitizes host cells for destruction by autologous complement. | lld:pubmed |
| pubmed-article:3084560 | pubmed:publicationType | Journal Article | lld:pubmed |
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