pubmed-article:18215992 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18215992 | lifeskim:mentions | umls-concept:C0004587 | lld:lifeskim |
pubmed-article:18215992 | lifeskim:mentions | umls-concept:C0042765 | lld:lifeskim |
pubmed-article:18215992 | lifeskim:mentions | umls-concept:C0028128 | lld:lifeskim |
pubmed-article:18215992 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
pubmed-article:18215992 | lifeskim:mentions | umls-concept:C0038952 | lld:lifeskim |
pubmed-article:18215992 | lifeskim:mentions | umls-concept:C0450254 | lld:lifeskim |
pubmed-article:18215992 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
pubmed-article:18215992 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:18215992 | pubmed:dateCreated | 2008-1-24 | lld:pubmed |
pubmed-article:18215992 | pubmed:abstractText | Phagocytes generate nitric oxide (NO) and other reactive oxygen and nitrogen species in large quantities to combat infecting bacteria. Here, we report the surprising observation that in vivo survival of a notorious pathogen-Bacillus anthracis-critically depends on its own NO-synthase (bNOS) activity. Anthrax spores (Sterne strain) deficient in bNOS lose their virulence in an A/J mouse model of systemic infection and exhibit severely compromised survival when germinating within macrophages. The mechanism underlying bNOS-dependent resistance to macrophage killing relies on NO-mediated activation of bacterial catalase and suppression of the damaging Fenton reaction. Our results demonstrate that pathogenic bacteria use their own NO as a key defense against the immune oxidative burst, thereby establishing bNOS as an essential virulence factor. Thus, bNOS represents an attractive antimicrobial target for treatment of anthrax and other infectious diseases. | lld:pubmed |
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pubmed-article:18215992 | pubmed:language | eng | lld:pubmed |
pubmed-article:18215992 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18215992 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:18215992 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18215992 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18215992 | pubmed:month | Jan | lld:pubmed |
pubmed-article:18215992 | pubmed:issn | 1091-6490 | lld:pubmed |
pubmed-article:18215992 | pubmed:author | pubmed-author:LippardStephe... | lld:pubmed |
pubmed-article:18215992 | pubmed:author | pubmed-author:NudlerEvgenyE | lld:pubmed |
pubmed-article:18215992 | pubmed:author | pubmed-author:GusarovIvanI | lld:pubmed |
pubmed-article:18215992 | pubmed:author | pubmed-author:ShatalinKonst... | lld:pubmed |
pubmed-article:18215992 | pubmed:author | pubmed-author:AvetissovaEka... | lld:pubmed |
pubmed-article:18215992 | pubmed:author | pubmed-author:McQuadeLindse... | lld:pubmed |
pubmed-article:18215992 | pubmed:author | pubmed-author:ShatalinaYele... | lld:pubmed |
pubmed-article:18215992 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:18215992 | pubmed:day | 22 | lld:pubmed |
pubmed-article:18215992 | pubmed:volume | 105 | lld:pubmed |
pubmed-article:18215992 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18215992 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18215992 | pubmed:pagination | 1009-13 | lld:pubmed |
pubmed-article:18215992 | pubmed:dateRevised | 2011-6-14 | lld:pubmed |
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pubmed-article:18215992 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:18215992 | pubmed:articleTitle | Bacillus anthracis-derived nitric oxide is essential for pathogen virulence and survival in macrophages. | lld:pubmed |
pubmed-article:18215992 | pubmed:affiliation | Department of Biochemistry, New York University School of Medicine, New York, NY 10016, USA. | lld:pubmed |
pubmed-article:18215992 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:18215992 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
pubmed-article:18215992 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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