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題名: | Interaction of Inflammatory and Anti-inflammatory Responses in Microglia by Staphylococcus Aureus-derived Lipoteichoic Acid |
作者: | Huang, Bor-Ren;Tsai, Cheng-Fang;Lin, Hsiao-Yun;Tseng, Wen-Pei;Huang, Shiang-Suo;Wu, Chi-Rei;Lin, Chingju;Yeh, Wei-Lan;Lu, Dah-Yuu |
貢獻者: | 運動健康所 |
關鍵詞: | Lipoteichoic acid;Microglia;Inflammation;Anti-inflammation;HO-1 |
日期: | 2013-05
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上傳時間: | 2014-01-15T04:02:54Z
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出版者: | Elsevier |
摘要: | We investigated the interaction between proinflammatory and inflammatory responses caused by Staphylococcus aureus-derived lipoteichoic acid (LTA) in primary cultured microglial cells and BV-2 microglia. LTA induced inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein levels increase in a concentration- and time-dependent manner. Meanwhile, LTA also increased nitric oxide (NO) and PGE2 production in microglia. Administration of TLR2 antagonist effectively inhibited LTA-induced NO, iNOS, and COX-2 expression. Moreover, treatment of cells with LTA caused a time-dependent activation of ERK, p38, JNK, as well as AKT. We also found that LTA-induced iNOS and COX-2 up-regulation were attenuated by p38, JNK, and PI3-kinase inhibitors. On the other hand, LTA-enhanced HO-1 expression was attenuated by p38 and PI3-kinase inhibitors. Treatment of cells with NF-κB and AP-1 inhibitors antagonized LTA-induced iNOS and COX-2 expression. However, only NF-κB inhibitors reduced LTA-induced HO-1 expression in microglia. Furthermore, stimulation of cells with LTA also activated IκBα phosphorylation, p65 phosphorylation at Ser536, and c-Jun phosphorylation. Moreover, LTA-induced increases of κB-DNA and AP-1-DNA binding activity were inhibited by p38, JNK, and PI3-kinase inhibitors. HO-1 activator CoPP IX dramatically reversed LTA-induced iNOS expression. Our results provided mechanisms linking LTA and inflammation/anti-inflammation, and indicated that LTA plays a regulatory role in microglia activation. |
關聯: | Toxicology and Applied Pharmacology, 269(1): 43-50 |
顯示於類別: | [運動健康研究所] 期刊論文
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