Dendritic cells (DCs) can mediate inflammation-related bone resorption that is crucial in the development of periodontitis. Butyrate is a critical by-product of microbes with antibacterial and anti-inflammatory properties. Here, we found that butyrate inhibited the activation of lipopolysaccharide (LPS)-induced DCs and generation of inflammatory cytokines by DCs. Moreover, butyrate regulated glycolysis in LPS-induced DCs via the G-protein-coupled receptor/hypoxia-inducible factor-1α pathway. In addition, butyrate inhibited the maturation of CD11c+MHC-II+ DCs in vivo, suppressing local inflammatory infiltration and ultimately alleviating bone resorption in a periodontitis model. Our results imply that butyrate suppresses the activation of LPS-induced DCs by modulating their metabolism, highlighting its potential as a therapeutic agent for inflammatory diseases.

中文翻译：

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丁酸盐抑制树突状细胞活化并减轻牙周炎。

树突状细胞（DC）可以介导炎症相关的骨吸收，这对于牙周炎的发展至关重要。丁酸盐是微生物的重要副产品，具有抗菌和抗炎特性。在这里，我们发现丁酸盐抑制脂多糖（LPS）诱导的 DC 的激活以及 DC 产生炎症细胞因子。此外，丁酸通过 G 蛋白偶联受体/缺氧诱导因子 1α 途径调节 LPS 诱导的 DC 中的糖酵解。此外，丁酸盐在体内抑制 CD11c+MHC-II+ DC 的成熟，抑制局部炎症浸润，最终减轻牙周炎模型中的骨吸收。我们的结果表明丁酸盐通过调节脂多糖诱导的树突状细胞的代谢来抑制其活化，突出了其作为炎症性疾病治疗剂的潜力。