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Published online before print March 23, 2004
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-induced TLR2 expression in murine hepatocytes
* Department of Molecular Health Sciences, Graduate School of Pharmaceutical Sciences, Nagoya City University, Japan;
Department of Pharmacology and Center for Pharmacogenetics, University of Pennsylvania School of Medicine, Philadelphia; and
Division of Cellular and Molecular Biology, Institute of Medical Science, University of Tokyo, Japan
1 Correspondence: Department of Molecular Health Sciences, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-dori, Mizuho-ku, Nagoya, Aichi 467-8603, Japan. E-mail: konozaki{at}phar.nagoya-cu.ac.jp
We have previously reported that the proinflammatory cytokine interleukin (IL)-1
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-ß (TGF-ß) on TLR2 expression in primary-cultured murine hepatocytes. At the mRNA and protein levels, TGF-ß up-regulated TLR2 expression but inhibited TLR2 expression induced by IL-1 at 24 h. BLP-induced SAA promoter activity could be augmented by pretreatment with IL-1 but not TGF-ß or the combination of TGF-ß and IL-1. TLR2 promoter activity and nuclear factor (NF)-
B activation by IL-1 were inhibited by TGF-ß treatment. Pretreatment with TGF-ß strongly suppressed IL-1-induced TLR2 promoter activity and NF-B activation, which was consistent with the down-regulation of type I IL-1 receptor (IL-1RI) mRNA expression. IL-1 up-regulated IL-1RI mRNA, but it was inhibited by the treatment with TGF-ß. These results suggest that TGF-ß suppresses the induction of TLR2 expression by IL-1 through down-regulation of IL-1RI expression. These results also demonstrate the disparity between IL-1 and TGF-ß in regulating TLR2-mediated SAA production in hepatocytes.
Key Words: bacterial lipopeptide • serum amyloid A • type I IL-1R
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