pubmed-article:8039877 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8039877 | lifeskim:mentions | umls-concept:C0348801 | lld:lifeskim |
pubmed-article:8039877 | lifeskim:mentions | umls-concept:C0028128 | lld:lifeskim |
pubmed-article:8039877 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
pubmed-article:8039877 | lifeskim:mentions | umls-concept:C0079785 | lld:lifeskim |
pubmed-article:8039877 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
pubmed-article:8039877 | lifeskim:mentions | umls-concept:C0851827 | lld:lifeskim |
pubmed-article:8039877 | lifeskim:mentions | umls-concept:C1701901 | lld:lifeskim |
pubmed-article:8039877 | lifeskim:mentions | umls-concept:C0591833 | lld:lifeskim |
pubmed-article:8039877 | lifeskim:mentions | umls-concept:C0441836 | lld:lifeskim |
pubmed-article:8039877 | pubmed:issue | 8 | lld:pubmed |
pubmed-article:8039877 | pubmed:dateCreated | 1994-8-24 | lld:pubmed |
pubmed-article:8039877 | pubmed:abstractText | Nitric oxide (NO) is produced by murine macrophages in response to cytokines and/or gram-negative bacterial lipopolysaccharide. NO induction by gram-positive bacteria such as group B streptococci (GBS), the major etiologic agents of neonatal pneumonia and meningitis, has received little study. GBS as well as two other gram-positive bacterial species, Staphylococcus aureus and Staphylococcus epidermidis, were found to stimulate NO production in thioglycolate-elicited murine macrophages and in the mouse macrophage cell line J774A.1 in the presence of gamma interferon. Serotype Ia and III GBS were both stimulatory, as were asialo- and type antigen-deficient mutant strains of type III GBS. NO production was dose dependent, inhibitable by L-arginine analogs, and unaffected by polymyxin B. Since phagocytosis by murine and human phagocytes of GBS is dependent on complement receptor type 3 (CR3), the role of CR3 in the NO response to GBS was tested in the CR3-deficient myelomonocytic cell line WEHI-3. GBS did not induce NO, whereas S. aureus or lipopolysaccharide did induce NO in WEHI-3 cells. S. epidermidis, whose nonopsonic phagocytosis is also CR3 dependent, failed to induce NO in WEHI-3 cells. Monoclonal anti-CR3 (anti-CD11b or anti-CD18) in the presence of interferon also induced NO production in thioglycolate-elicited macrophages and in J774A.1 cells but not in WEHI-3 cells. This evidence suggests that ligated CR3 and gamma interferon act synergistically to induce NO production and that CR3 mediates the GBS-induced signal for NO production in interferon-treated macrophages. | lld:pubmed |
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pubmed-article:8039877 | pubmed:language | eng | lld:pubmed |
pubmed-article:8039877 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8039877 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:8039877 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8039877 | pubmed:month | Aug | lld:pubmed |
pubmed-article:8039877 | pubmed:issn | 0019-9567 | lld:pubmed |
pubmed-article:8039877 | pubmed:author | pubmed-author:GoodrumK JKJ | lld:pubmed |
pubmed-article:8039877 | pubmed:author | pubmed-author:SchneiderBB | lld:pubmed |
pubmed-article:8039877 | pubmed:author | pubmed-author:McCormickL... | lld:pubmed |
pubmed-article:8039877 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8039877 | pubmed:volume | 62 | lld:pubmed |
pubmed-article:8039877 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8039877 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8039877 | pubmed:pagination | 3102-7 | lld:pubmed |
pubmed-article:8039877 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:8039877 | pubmed:year | 1994 | lld:pubmed |
pubmed-article:8039877 | pubmed:articleTitle | Group B streptococcus-induced nitric oxide production in murine macrophages is CR3 (CD11b/CD18) dependent. | lld:pubmed |
pubmed-article:8039877 | pubmed:affiliation | Department of Biological Sciences, Ohio University, Athens 45701-2979. | lld:pubmed |
pubmed-article:8039877 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:8039877 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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