KMID : 0603820160220020060
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Journal of Experimental & Biomedical Science 2016 Volume.22 No. 2 p.60 ~ p.64
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S100A8 Induces Secretion of MCP-1, IL-6, and IL-8 via TLR4 in Jurkat T Cells
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Nam A-Reum
Kim Da-Hae Kim Mun-Jeong Lee Ji-Sook Yang Seung-Ju Kim In-Sik
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Abstract
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In the pathogenesis of inflammatory diseases such as allergies, S100A8 acts as an important molecule and T lymphocytes are essential cytokine-releasing cells. In this study, we investigated the effect of S100A8 on release of cytokines, specifically MCP-1, IL-6, and IL-8 in T cells, and its associated signaling mechanism. S100A8 increased secretion of MCP-1, IL-6, and IL-8 in a time- and dose-dependent manner. Elevated secretion of MCP-1, IL-6, and IL-8 due to S100A8 was inhibited by the TLR4 inhibitor TLR4i, the PI3K inhibitor LY294002, the PKC¥ä inhibitor rottlerin, the ERK inhibitor PD98059, the p38 MAPK inhibitor SB202190, the JNK inhibitor SP600125, and the NF-¥êB inhibitor BAY-11-7085. S100A8 induced phosphorylation of ERK, p38 MAPK, and JNK in a time-dependent manner, and activation was suppressed by TLR4i, LY294002, and rottlerin. S100A8 induced NF-¥êB activation by I¥ê-B¥á degradation, and NF-¥êB activity was suppressed by PD98059, SB202190, and SP600125. These results indicate that S100A8 induces cytokine release via TLR4. Study of PI3K, PKC¥ä, MAPKs, and NF-¥êB will contribute to elucidation of the S100A8-invovled mechanism.
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KEYWORD
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S100A8 , Lymphocytes , Cytokine , TLR4
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