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rdf:type |
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lifeskim:mentions |
umls-concept:C0009319,
umls-concept:C0011195,
umls-concept:C0017641,
umls-concept:C0021368,
umls-concept:C0021853,
umls-concept:C0026809,
umls-concept:C0037473,
umls-concept:C0086140,
umls-concept:C0205263,
umls-concept:C0441655,
umls-concept:C0521447,
umls-concept:C0719637,
umls-concept:C1848296,
umls-concept:C2698419,
umls-concept:C2698698
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pubmed:issue |
1
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pubmed:dateCreated |
2000-5-8
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pubmed:abstractText |
In acute DSS-induced colitis nuclear factor (NF)-kappaB-dependent inflammatory cytokines including IL-1 and tumour necrosis factor-alpha (TNF-alpha) are up-regulated. Here we examined the effects of gliotoxin, a fungal metabolite known to inhibit NF-kappaB activity, on cytokine production by a mouse cell system in vitro and on intestinal inflammation and NF-kappaB activation in vivo. In vitro gliotoxin decreased TNF-alpha gene expression and protein production by RAW-264.7 mouse macrophage-like cells stimulated with lipopolysaccharide. In vivo, gliotoxin treatment of mice was begun on day 3 of 5% DSS application dissolved in the drinking water and continued until day 8. Gliotoxin treatment dose-dependently down-regulated colonic inflammation as assessed histologically and in parallel there was a suppression of colonic TNF-alpha and IL-1alpha mRNA expression on day 8 as analysed by semiquantitative reverse transcriptase-polymerase chain reaction (P < 0.01). Furthermore, colonic NF-kappaB DNA-binding activity was increased in DSS-induced colitis and was suppressed by gliotoxin. These results demonstrate the essential role of NF-kappaB in DSS-induced colitis and indicate a molecular approach to the treatment of intestinal inflammatory disorders.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-1670578,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-1688816,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-2422547,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-2426570,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-2430903,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-2433961,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-2787769,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-6203127,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-6286012,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-7510665,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-7557106,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-7806062,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-7900941,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-7958674,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-8566866,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-8601637,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-8666939,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-8683390,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-8717528,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-8777967,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-8782457,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-8801200,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-9030875,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-9038666,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-9091804,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-9304400,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-9316879,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-9523521,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-9530156,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-9550432,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-9551998,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-9597130,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-9616307,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-9679041,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-9691914,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-9705531,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-9811891,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-9822251,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-9872503,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10759764-9878126
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0009-9104
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
120
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
59-65
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:10759764-Animals,
pubmed-meshheading:10759764-Cell Line,
pubmed-meshheading:10759764-Colitis,
pubmed-meshheading:10759764-Dextran Sulfate,
pubmed-meshheading:10759764-Female,
pubmed-meshheading:10759764-Gene Expression Regulation,
pubmed-meshheading:10759764-Gliotoxin,
pubmed-meshheading:10759764-Immunosuppressive Agents,
pubmed-meshheading:10759764-Injections, Intraperitoneal,
pubmed-meshheading:10759764-Interleukin-1,
pubmed-meshheading:10759764-Mice,
pubmed-meshheading:10759764-Mice, Inbred BALB C,
pubmed-meshheading:10759764-NF-kappa B,
pubmed-meshheading:10759764-Tumor Necrosis Factor-alpha,
pubmed-meshheading:10759764-Up-Regulation
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pubmed:year |
2000
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pubmed:articleTitle |
Nuclear factor-kappa B activity and intestinal inflammation in dextran sulphate sodium (DSS)-induced colitis in mice is suppressed by gliotoxin.
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