Source:http://linkedlifedata.com/resource/pubmed/id/18768878
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6
|
| pubmed:dateCreated |
2008-9-4
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| pubmed:abstractText |
Cecal ligation and puncture (CLP) caused septic peritonitis in wild-type (WT) mice, with approximately 33% mortality within 7 days after the procedure. Concomitantly, the protein level of intraperitoneal CX3CL1/fractalkine was increased, with infiltration by CX3CR1-expressing macrophages into the peritoneum. CLP induced 75% mortality in CX3CR1-deficient (CX3CR1(-/-)) mice, which, however, exhibited a similar degree of intraperitoneal leukocyte infiltration as WT mice. Despite this, CX3CR1(-/-) mice exhibited impairment in intraperitoneal bacterial clearance, together with a reduction in the expression of intraperitoneal inducible NO synthase (iNOS) and bactericidal proinflammatory cytokines, including IL-1beta, TNF-alpha, IFN-gamma, and IL-12, compared with WT mice. Bactericidal ability of peritoneal phagocytes such as neutrophils and macrophages was consistently attenuated in CX3CR1(-/-) mice compared with WT mice. Moreover, when WT macrophages were stimulated in vitro with CX3CL1, their bactericidal activity was augmented in a dose-dependent manner, with enhanced iNOS gene expression and subsequent NO generation. Furthermore, CX3CL1 enhanced the gene expression of IL-1beta, TNF-alpha, IFN-gamma, and IL-12 by WT macrophages with NF-kappaB activation. Thus, CX3CL1-CX3CR1 interaction is crucial for optimal host defense against bacterial infection by activating bacterial killing functions of phagocytes, and by augmenting iNOS-mediated NO generation and bactericidal proinflammatory cytokine production mainly through the NF-kappaB signal pathway, with few effects on macrophage infiltration.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Sep
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| pubmed:issn |
1550-6606
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:day |
15
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| pubmed:volume |
181
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
4208-18
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:18768878-Animals,
pubmed-meshheading:18768878-Blood Bactericidal Activity,
pubmed-meshheading:18768878-Cecum,
pubmed-meshheading:18768878-Cells, Cultured,
pubmed-meshheading:18768878-Cytokines,
pubmed-meshheading:18768878-Disease Models, Animal,
pubmed-meshheading:18768878-Escherichia coli Infections,
pubmed-meshheading:18768878-Genetic Predisposition to Disease,
pubmed-meshheading:18768878-Immunity, Innate,
pubmed-meshheading:18768878-Inflammation Mediators,
pubmed-meshheading:18768878-Ligation,
pubmed-meshheading:18768878-Macrophages, Peritoneal,
pubmed-meshheading:18768878-Male,
pubmed-meshheading:18768878-Mice,
pubmed-meshheading:18768878-Mice, Inbred C57BL,
pubmed-meshheading:18768878-Mice, Knockout,
pubmed-meshheading:18768878-Neutrophil Infiltration,
pubmed-meshheading:18768878-Peritonitis,
pubmed-meshheading:18768878-Punctures,
pubmed-meshheading:18768878-Receptors, Chemokine,
pubmed-meshheading:18768878-Shock, Septic,
pubmed-meshheading:18768878-Signal Transduction
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| pubmed:year |
2008
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| pubmed:articleTitle |
Essential involvement of CX3CR1-mediated signals in the bactericidal host defense during septic peritonitis.
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| pubmed:affiliation |
Department of Forensic Medicine and.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|