Source:http://linkedlifedata.com/resource/pubmed/id/10975994
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
2000-10-10
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pubmed:abstractText |
Alveolar macrophages are an important source of inflammatory cytokines in the lung. IL-10 has been shown to inhibit inflammatory cytokine production by human alveolar macrophages, but mechanisms are unclear. The purpose of the present study was to investigate whether IL-10 modified cytokine production by interference with transcriptional pathways. Alveolar macrophages were obtained from healthy controls by fiberoptic bronchoscopy and incubated with LPS+/-IL-10. Results indicated that steady state mRNA levels of tumour necrosis factor-alpha (TNF) and interleukin 1-beta (IL-1) decreased in the presence of IL-10. Consequently, electrophoretic mobility shift assays were performed using end-labelled nuclear factor-kappa B (NF-kappa B) or activator protein-1 (AP-1) probe. NF-kappa B binding was decreased in extracts from macrophages incubated for 4 h with LPS+IL-10 in comparison to those incubated with LPS alone. IL-10 also inhibited TNF secretion and NF-kappa B activation induced by another stimulus, staphylococcal toxin. Supershift assays revealed the presence of both p50 and p65 subunits of NF-kappa B. AP-1 was not affected by IL-10. Further examination of mechanisms indicated that IL-10 delayed the LPS-mediated degradation of the inhibitor protein I kappa B, thus delaying the nuclear translocation of the p65 subunit. These observations provide the first evidence that IL-10 antagonizes cytokine transcription in human alveolar macrophages by impeding the nuclear translocation of NF-kappa B by delaying the degradation of I kappa B.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Enterotoxins,
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/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor RelA,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/enterotoxin B, staphylococcal
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1043-4666
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 2000 Academic Press.
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pubmed:issnType |
Print
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pubmed:volume |
12
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1348-55
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:10975994-Blotting, Western,
pubmed-meshheading:10975994-Cell Nucleus,
pubmed-meshheading:10975994-Cytokines,
pubmed-meshheading:10975994-Enterotoxins,
pubmed-meshheading:10975994-Humans,
pubmed-meshheading:10975994-I-kappa B Proteins,
pubmed-meshheading:10975994-Interleukin-1,
pubmed-meshheading:10975994-Interleukin-10,
pubmed-meshheading:10975994-Lipopolysaccharides,
pubmed-meshheading:10975994-Lung,
pubmed-meshheading:10975994-Macrophages, Alveolar,
pubmed-meshheading:10975994-Microscopy, Fluorescence,
pubmed-meshheading:10975994-NF-kappa B,
pubmed-meshheading:10975994-RNA, Messenger,
pubmed-meshheading:10975994-Transcription, Genetic,
pubmed-meshheading:10975994-Transcription Factor RelA,
pubmed-meshheading:10975994-Tumor Necrosis Factor-alpha
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pubmed:year |
2000
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pubmed:articleTitle |
Interleukin 10 (IL-10)-mediated inhibition of inflammatory cytokine production by human alveolar macrophages.
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pubmed:affiliation |
Department of Pulmonary and Critical Care Medicine, The Cleveland Clinic Foundation, 9500 Euclid Avenue Cleveland, Ohio 44195-5038, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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