High-mobility group box protein-1 released by human-periodontal ligament cells modulates macrophage migration and activity in vitro
High-mobility group box protein-1 released by human-periodontal ligament cells modulates macrophage migration and activity in vitro
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DOI：
10.1177/1753425913505121
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发表时间：
2014-10
期刊：
影响因子：
3.2
通讯作者：
M. Wolf;S. Lossdörfer;R. Craveiro;A. Jäger
中科院分区：
文献类型：
--
作者：
M. Wolf;S. Lossdörfer;R. Craveiro;A. Jäger
最近的研究表明，在组织修复过程中，人牙周膜细胞（hPDL）与免疫细胞（如巨噬细胞）相互作用。高迁移率族蛋白-1（HMGB 1）由受损细胞释放到细胞外环境中，并作为警报蛋白介导炎症宿主反应。本研究探讨了人牙周膜细胞释放的HMGB 1对巨噬细胞分化、迁移和活动的调节作用。目的是检查HMGB 1本身以及与其他介质组合的炎症潜力。通过免疫细胞化学/ELISA测定，通过热损伤诱导hPDL无菌坏死导致HMGB 1从细胞核易位到细胞质和细胞外空间。人巨噬细胞暴露于条件PDL细胞培养基增加了巨噬细胞分化/活化标志物CD 14、CD 23、CD 64和CD 163的表达。巨噬细胞趋化迁移和成骨分化也增强。用饱和浓度的HMGB 1-Ab补充条件培养基可降低这些作用。与热损伤相比，重组HMGB 1蛋白的挑战诱导较少的迁移和破骨细胞分化。这些数据表明hPDL通过释放介质（包括HMGB 1）的免疫调节能力，所述介质在牙周修复期间改变巨噬细胞分化、迁移和活性，并且表明当与其他介质协同作用时增强的HMGB 1活性。
Recent studies have demonstrated the interplay of human periodontal ligament cells (hPDLs) with immune cells, such as macrophages, during tissue repair. High-mobility group box protein-1 (HMGB1) is released into the extracellular milieu by damaged cells and functions as an alarmin to mediate the inflammatory host response. The present study addressed the role of HMGB1 released by hPDLs in the regulation of macrophage differentiation, migration and activity. The aim was to examine the inflammatory potential of HMGB1 itself and in combination with other mediators. The induction of sterile necrosis by thermal insult of hPDLs resulted in HMGB1 translocation from the nucleus to the cytoplasm and on to the extracellular space, as determined by immunocytochemistry/ELISA. Exposure of human macrophages to the conditioned PDL cell medium increased the expression of macrophage differentiation/activation markers CD14, CD23, CD64 and CD163. Chemotactic migration and osteoclastic differentiation of macrophages were also enhanced. Supplementation of the conditioned medium with a saturating concentration of HMGB1-Ab reduced these effects. Challenge with recombinant HMGB1 protein induced less migration and osteoclast differentiation than thermal insult. These data point to the immune modulatory capacity of hPDLs by the release of mediators, including HMGB1, which modify macrophage differentiation, migration and activity during periodontal repair, and indicate an enhanced HMGB1 activity when acting in concert with other mediators.