Source:http://linkedlifedata.com/resource/pubmed/id/10521084
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
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| pubmed:dateCreated |
1999-10-25
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| pubmed:abstractText |
Recent studies support nuclear factor-kappaB (NF-kappaB) as a critical transcription factor in inflammatory bowel disease. We examined NF-kappaB and its inhibitors, IkappaB-alpha and IkappaB-beta, in the colitis of interleukin-2 deficient (IL-2-/-) mice at the ages of 5, 10, and 15 weeks and compared them with those of age-matched wild-type mice. Colon levels of nuclear NF-kappaB and mRNA for NF-kappaB responsive cytokines interleukin-1beta and tumor necrosis factor-alpha were markedly increased in interleukin-2-/-mice. Colon interleukin-1beta protein levels were significantly elevated, consistent with increased interleukin-1beta mRNA, whereas tumor necrosis factor-alpha protein levels were either lower than those of the control group or did not differ. Protein levels of the immunomodulatory cytokine interleukin-10 were diminished. The NF-kappaB responsive IkappaB-alpha was also increased, mirroring NF-kappaB activation. In contrast, IkappaB-beta levels did not differ from those of wild-type mice in the 5- and 10-week groups and were only mildly increased in the 15-week group. Serum amyloid A, an acute phase protein that also is NF-kappaB-responsive, was dramatically elevated in the serum of interleukin-2-/- mice and correlated with the severity of the colitis. These data support a role for NF-kappaB in the pathogenesis of intestinal inflammation in interleukin-2-/- mice. The measurement of NF-kappaB in colon tissue samples may provide a sensitive means of assessing the state of activation of the mucosal immune response, and serum amyloid A appears to be a reliable biochemical marker of disease activity.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Biological Markers,
http://linkedlifedata.com/resource/pubmed/chemical/I-kappa B Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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| pubmed:status |
MEDLINE
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| pubmed:month |
Oct
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| pubmed:issn |
0022-2143
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
134
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
378-85
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| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:10521084-Acute-Phase Reaction,
pubmed-meshheading:10521084-Animals,
pubmed-meshheading:10521084-Biological Markers,
pubmed-meshheading:10521084-Cell Nucleus,
pubmed-meshheading:10521084-Colitis, Ulcerative,
pubmed-meshheading:10521084-Cytosol,
pubmed-meshheading:10521084-Female,
pubmed-meshheading:10521084-Gene Expression,
pubmed-meshheading:10521084-Genotype,
pubmed-meshheading:10521084-I-kappa B Proteins,
pubmed-meshheading:10521084-Interleukin-1,
pubmed-meshheading:10521084-Interleukin-10,
pubmed-meshheading:10521084-Interleukin-2,
pubmed-meshheading:10521084-Male,
pubmed-meshheading:10521084-Mice,
pubmed-meshheading:10521084-Mice, Inbred C57BL,
pubmed-meshheading:10521084-Mice, Mutant Strains,
pubmed-meshheading:10521084-NF-kappa B,
pubmed-meshheading:10521084-RNA, Messenger,
pubmed-meshheading:10521084-Rectal Prolapse,
pubmed-meshheading:10521084-Tumor Necrosis Factor-alpha
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| pubmed:year |
1999
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| pubmed:articleTitle |
Increased nuclear factor-kappaB activation in colitis of interleukin-2-deficient mice.
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| pubmed:affiliation |
Department of Internal Medicine, University of Kentucky, Lexington, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.
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