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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2004-6-3
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pubmed:abstractText |
We have previously reported that the proinflammatory cytokine interleukin (IL)-1alpha can up-regulate functional Toll-like receptor 2 (TLR2) expression in primary-cultured murine hepatocytes, and bacterial lipopeptide (BLP) is capable of signaling through TLR2 to induce serum amyloid A (SAA) expression in hepatocytes. In the present study, we investigated the effect of the anti-inflammatory cytokine transforming growth factor-beta (TGF-beta) on TLR2 expression in primary-cultured murine hepatocytes. At the mRNA and protein levels, TGF-beta up-regulated TLR2 expression but inhibited TLR2 expression induced by IL-1alpha at 24 h. BLP-induced SAA promoter activity could be augmented by pretreatment with IL-1alpha but not TGF-beta or the combination of TGF-beta and IL-1alpha. TLR2 promoter activity and nuclear factor (NF)-kappaB activation by IL-1alpha were inhibited by TGF-beta treatment. Pretreatment with TGF-beta strongly suppressed IL-1alpha-induced TLR2 promoter activity and NF-kappaB activation, which was consistent with the down-regulation of type I IL-1 receptor (IL-1RI) mRNA expression. IL-1alpha up-regulated IL-1RI mRNA, but it was inhibited by the treatment with TGF-beta. These results suggest that TGF-beta suppresses the induction of TLR2 expression by IL-1alpha through down-regulation of IL-1RI expression. These results also demonstrate the disparity between IL-1alpha and TGF-beta in regulating TLR2-mediated SAA production in hepatocytes.
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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 |
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-1 Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Serum Amyloid A Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 2,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptors,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0741-5400
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
75
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1056-61
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:15039464-Animals,
pubmed-meshheading:15039464-Apolipoproteins,
pubmed-meshheading:15039464-Down-Regulation,
pubmed-meshheading:15039464-Female,
pubmed-meshheading:15039464-Hepatocytes,
pubmed-meshheading:15039464-Interleukin-1,
pubmed-meshheading:15039464-Membrane Glycoproteins,
pubmed-meshheading:15039464-Mice,
pubmed-meshheading:15039464-Mice, Inbred ICR,
pubmed-meshheading:15039464-NF-kappa B,
pubmed-meshheading:15039464-Promoter Regions, Genetic,
pubmed-meshheading:15039464-RNA, Messenger,
pubmed-meshheading:15039464-Receptors, Cell Surface,
pubmed-meshheading:15039464-Receptors, Interleukin-1,
pubmed-meshheading:15039464-Receptors, Interleukin-1 Type I,
pubmed-meshheading:15039464-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:15039464-Serum Amyloid A Protein,
pubmed-meshheading:15039464-Toll-Like Receptor 2,
pubmed-meshheading:15039464-Toll-Like Receptors,
pubmed-meshheading:15039464-Transforming Growth Factor beta
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pubmed:year |
2004
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pubmed:articleTitle |
TGF-beta down-regulates IL-1alpha-induced TLR2 expression in murine hepatocytes.
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pubmed:affiliation |
Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-dori, Mizuho-ku, Nagoya, Aichi 467-8603, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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