丁酸盐
炎症
牙周炎
化学
脂多糖
树突状细胞
CD11c公司
细胞生物学
免疫学
医学
生物
免疫系统
生物化学
内科学
发酵
基因
表型
作者
Lili Wu,Zhenhua Luo,Yu Chen,Ziqi Yan,Jing Fu,Yiyang Jiang,Junji Xu,Ye Liu
标识
DOI:10.1177/00220345231187824
摘要
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.
科研通智能强力驱动
Strongly Powered by AbleSci AI