Source:http://linkedlifedata.com/resource/pubmed/id/11342656
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
10
|
| pubmed:dateCreated |
2001-5-8
|
| pubmed:abstractText |
To determine the role of endogenous IL-10 in local antibacterial host defense and in the development of a systemic inflammatory response syndrome during abdominal sepsis, IL-10 gene-deficient (IL-10(-/-)) and wild-type (IL-10(+/+)) mice received an i.p. injection with Escherichia coli. Peritonitis was associated with a bacterial dose-dependent increase in IL-10 concentrations in peritoneal fluid and plasma. The recovery of E. coli from the peritoneal fluid, blood, and lungs was diminished in IL-10(-/-) mice, indicating that endogenous IL-10 impaired bacterial clearance. Despite a lower bacterial load, IL-10(-/-) mice had higher concentrations of TNF, macrophage inflammatory protein-2 and keratinocyte in peritoneal fluid and plasma, and demonstrated more severe multiple organ damage as indicated by clinical chemistry and histopathology. Furthermore, IL-10(-/-) mice showed an increased neutrophil recruitment to the peritoneal cavity. To examine the role of elevated TNF levels in the altered host response in IL-10(-/-) mice, the effect of a neutralizing anti-TNF mAb was determined. Anti-TNF did not influence the clearance of E. coli in either IL-10(+/+) or IL-10(-/-) mice. Furthermore, anti-TNF did not affect leukocyte influx in the peritoneal fluid, multiple organ damage, or survival in IL-10(+/+) mice. In IL-10(-/-) mice, anti-TNF partially attenuated neutrophil recruitment and multiple organ damage, and prevented the increased lethality. These data suggest that although endogenous IL-10 facilitates the outgrowth and dissemination of bacteria during E. coli peritonitis, it protects mice from lethality by attenuating the development of a systemic inflammatory response syndrome by a mechanism that involves inhibition of TNF release.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
May
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| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
15
|
| pubmed:volume |
166
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
6323-31
|
| pubmed:dateRevised |
2008-11-21
|
| pubmed:meshHeading |
pubmed-meshheading:11342656-Animals,
pubmed-meshheading:11342656-Ascitic Fluid,
pubmed-meshheading:11342656-Chemokines,
pubmed-meshheading:11342656-Colony Count, Microbial,
pubmed-meshheading:11342656-Escherichia coli,
pubmed-meshheading:11342656-Escherichia coli Infections,
pubmed-meshheading:11342656-Immunity, Innate,
pubmed-meshheading:11342656-Interleukin-10,
pubmed-meshheading:11342656-Male,
pubmed-meshheading:11342656-Mice,
pubmed-meshheading:11342656-Mice, Inbred C57BL,
pubmed-meshheading:11342656-Mice, Knockout,
pubmed-meshheading:11342656-Multiple Organ Failure,
pubmed-meshheading:11342656-Neutrophil Infiltration,
pubmed-meshheading:11342656-Peritoneal Cavity,
pubmed-meshheading:11342656-Peritonitis,
pubmed-meshheading:11342656-Survival Rate,
pubmed-meshheading:11342656-Tumor Necrosis Factor-alpha
|
| pubmed:year |
2001
|
| pubmed:articleTitle |
IL-10-deficient mice demonstrate multiple organ failure and increased mortality during Escherichia coli peritonitis despite an accelerated bacterial clearance.
|
| pubmed:affiliation |
Department of Surgery, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|