| pubmed-article:1908513 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1908513 | lifeskim:mentions | umls-concept:C0004611 | lld:lifeskim |
| pubmed-article:1908513 | lifeskim:mentions | umls-concept:C1819995 | lld:lifeskim |
| pubmed-article:1908513 | lifeskim:mentions | umls-concept:C0178719 | lld:lifeskim |
| pubmed-article:1908513 | lifeskim:mentions | umls-concept:C0679199 | lld:lifeskim |
| pubmed-article:1908513 | lifeskim:mentions | umls-concept:C1880266 | lld:lifeskim |
| pubmed-article:1908513 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:1908513 | pubmed:dateCreated | 1991-9-26 | lld:pubmed |
| pubmed-article:1908513 | pubmed:abstractText | The rate of growth of Listeria monocytogenes in the livers of mice infected intravenously with a lethal or sublethal inoculum of this facultative intracellular bacterium is greatly increased if neutrophils and other host cells are prevented from accumulating at foci of infection during the first 24 h by treatment with a monoclonal antibody (5C6) specific for the type 3 complement receptor of myelomonocytic cells. A histological examination of the livers of control mice showed that the accumulation of neutrophils at infectious foci resulted in the focal destruction of infected hepatocytes. In contrast, failure of neutrophils to accumulate at these sites in 5C6-treated mice allowed Listeria to multiply extensively in hepatocytes without destroying them. The results indicate that neutrophils play an important role in early defense against listeriosis in the liver by destroying infected hepatocytes, thereby reducing the opportunity for Listeria to multiply in permissive cells. In this way, neutrophils serve to break the chain of cell-to-cell spread of infection. | lld:pubmed |
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| pubmed-article:1908513 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1908513 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1908513 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1908513 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1908513 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:1908513 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:1908513 | pubmed:author | pubmed-author:NorthR JRJ | lld:pubmed |
| pubmed-article:1908513 | pubmed:author | pubmed-author:ConlanJ WJW | lld:pubmed |
| pubmed-article:1908513 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1908513 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:1908513 | pubmed:volume | 174 | lld:pubmed |
| pubmed-article:1908513 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1908513 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1908513 | pubmed:pagination | 741-4 | lld:pubmed |
| pubmed-article:1908513 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:1908513 | pubmed:year | 1991 | lld:pubmed |
| pubmed-article:1908513 | pubmed:articleTitle | Neutrophil-mediated dissolution of infected host cells as a defense strategy against a facultative intracellular bacterium. | lld:pubmed |
| pubmed-article:1908513 | pubmed:affiliation | Trudeau Institute, Inc., Saranac Lake, New York 12983. | lld:pubmed |
| pubmed-article:1908513 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1908513 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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