Source:http://linkedlifedata.com/resource/pubmed/id/14693703
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2003-12-24
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| pubmed:abstractText |
Interleukin (IL)-1 beta and IL-18 are two cytokines associated with the immunopathogenesis of diabetes in NOD mice. Both of these cytokines are cleaved by caspase-1 to their biologically active forms. IL-1 is a proinflammatory cytokine linked to beta-cell damage, and IL-18 stimulates production of interferon (IFN)gamma in synergy with IL-12. To examine the effects produced by caspase-1 deficiency on diabetes development in NOD/Lt mice, a disrupted Casp1 gene was introduced by a speed congenic technique. Casp1(-/-) bone marrow-derived macrophages stimulated with lipopolysaccharide produced no detectable IL-18, fourfold lower IL-1 beta, and 20-30% less IL-1 alpha than macrophages from wild-type Casp1(+/+) or Casp1(+/-) controls. Unexpectedly, despite reduced IL-1 and IL-18, there was no change in the rate of diabetes or in total incidence as compared with that in wild-type NOD mice. IL-1 reportedly makes an important pathological contribution in the multidose streptozotocin model of diabetes; however, there was no difference in sensitivity to streptozotocin between NOD mice and NOD.Casp1(-/-) mice at 40 mg/kg body wt or at 25 mg/kg body wt dosage levels. These findings show that caspase-1 processing of IL-1 beta and IL-18 is not absolutely required for mediation of spontaneous or chemically induced diabetes pathogenesis in the NOD mouse.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-18,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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| pubmed:status |
MEDLINE
|
| pubmed:month |
Jan
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| pubmed:issn |
0012-1797
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| pubmed:author |
pubmed-author:ChervonskyAlexander VAV,
pubmed-author:Choisy-RossiCaroline MorganeCM,
pubmed-author:HaskellBradford DBD,
pubmed-author:LeiterEdward HEH,
pubmed-author:MiltonMartha JMJ,
pubmed-author:PiganelliJon DJD,
pubmed-author:ReifsnyderPeter CPC,
pubmed-author:SchottWilliam HWH,
pubmed-author:TseHubert MHM
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| pubmed:issnType |
Print
|
| pubmed:volume |
53
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
99-104
|
| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:14693703-Animals,
pubmed-meshheading:14693703-Caspase 1,
pubmed-meshheading:14693703-Diabetes Mellitus, Experimental,
pubmed-meshheading:14693703-Diabetes Mellitus, Type 1,
pubmed-meshheading:14693703-Female,
pubmed-meshheading:14693703-Incidence,
pubmed-meshheading:14693703-Interleukin-1,
pubmed-meshheading:14693703-Interleukin-18,
pubmed-meshheading:14693703-Kinetics,
pubmed-meshheading:14693703-Lipopolysaccharides,
pubmed-meshheading:14693703-Macrophages,
pubmed-meshheading:14693703-Male,
pubmed-meshheading:14693703-Mice,
pubmed-meshheading:14693703-Mice, Inbred NOD,
pubmed-meshheading:14693703-Mice, Knockout,
pubmed-meshheading:14693703-Sex Characteristics,
pubmed-meshheading:14693703-Species Specificity,
pubmed-meshheading:14693703-Tumor Necrosis Factor-alpha
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| pubmed:year |
2004
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| pubmed:articleTitle |
Caspase-1 is not required for type 1 diabetes in the NOD mouse.
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| pubmed:affiliation |
The Jackson Laboratory, Bar Harbor, Maine 04609, USA.
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| pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|