Yan Xiaodong, Yuan Zhiyao, Bian Yifeng, Jin Lei, Mao Zhao, Lei Jiang, Chen Ning
Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
Department of Stomatology, Jinling Hospital, Medical School of Nanjing University, Nanjing, China.
Cent Eur J Immunol. 2020;45(1):9-21. doi: 10.5114/ceji.2020.94664.
Periodontitis is an inflammatory disease accompanied by alveolar bone loss. Moreover, M1 macrophages play a critical role in the development of periodontal disease. Uncoupling protein-2 (UCP2) is a mitochondrial transporter protein that controls M1 macrophage activation by modulating reactive oxygen species (ROS) production. We investigated the role of UCP2 in M1 macrophage infiltration in gingival tissues with periodontitis. We found that the expression of UCP2 was upregulated in M1 macrophages infiltrating human periodontal tissues with periodontitis. Macrophage-specific knockout of UCP2 could increase the infiltration of macrophage and exacerbate inflammatory response in a mouse gingiva affected with periodontitis, induced by Porphyromonas gingivalis-LPS (Pg-LPS) injection. The loss of UCP2 may contribute to the enhanced abilities of proliferation, migration, pro-inflammatory cytokine secretion, and ROS production in Pg-LPS-treated macrophages. Our results indicate that UCP2 has an important role in M1 macrophage polarization in the periodontal tissue with periodontitis. It might be helpful to provide theoretical basis for design of new therapeutic strategies for periodontitis.
牙周炎是一种伴有牙槽骨丧失的炎症性疾病。此外，M1巨噬细胞在牙周疾病的发展中起关键作用。解偶联蛋白2（UCP2）是一种线粒体转运蛋白，通过调节活性氧（ROS）的产生来控制M1巨噬细胞的激活。我们研究了UCP2在牙周炎牙龈组织中M1巨噬细胞浸润中的作用。我们发现，在浸润患有牙周炎的人类牙周组织的M1巨噬细胞中，UCP2的表达上调。巨噬细胞特异性敲除UCP2可增加巨噬细胞的浸润，并加剧牙龈卟啉单胞菌脂多糖（Pg-LPS）注射诱导的小鼠牙周炎牙龈中的炎症反应。UCP2的缺失可能有助于增强Pg-LPS处理的巨噬细胞的增殖、迁移、促炎细胞因子分泌和ROS产生能力。我们的结果表明，UCP2在牙周炎牙周组织中M1巨噬细胞极化中起重要作用。这可能有助于为牙周炎新治疗策略的设计提供理论依据。
