Force-induced IL-8 from periodontal ligament cells requires IL-1β

Force-induced IL-8 from periodontal ligament cells requires IL-1β
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DOI:
10.1177/154405910708600709
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发表时间:
2007-07-01
影响因子:
7.6
通讯作者:
Matsuguchi, T.
Matsuguchi, T.
中科院分区:
医学1区
文献类型:
--
作者:
Maeda, A.;Soejima, K.;Matsuguchi, T.

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在正畸牙齿移动过程中,机械应力会引起牙周膜(PDL)的炎症反应。我们假设机械应力下 PDL 细胞释放的趋化因子调节破骨细胞生成,并研究了人 PDL 细胞响应机械应力的趋化因子表达谱和机制。在体外,剪切应力和压力迅速增加PDL细胞的IL-8/CXCL8基因和蛋白表达。一致地,健康个体龈沟液中 IL-8 的含量在正畸力应用后 2 至 4 天内增加。 PDL 细胞组成性表达低水平的 IL-1β,机械应力不会进一步增加这种水平。有趣的是,IL-1β的中和消除了机械应力对IL-8的诱导,表明IL-1β对于IL-8诱导至关重要,可能是通过自分泌或旁分泌机制。最后,信号特异性抑制剂的实验表明 MAP 激酶激活对于 IL-8 诱导至关重要。
During orthodontic tooth movement, mechanical stresses induce inflammatory reactions in the periodontal ligament (PDL). We hypothesized that chemokines released from PDL cells under mechanical stress regulate osteoclastogenesis, and investigated the profiles and mechanisms of chemokine expression by human PDL cells in response to mechanical stress. In vitro, shear stress and pressure force rapidly increased the gene and protein expressions of IL-8/CXCL8 by PDL cells. Consistently, amounts of IL-8 in the gingival crevicular fluid of healthy individuals increased within 2 to 4 days of orthodontic force application. The PDL cells constitutively expressed low levels of IL-1 beta, which were not further increased by mechanical stress. Interestingly, neutralization of IL-1 beta abolished IL-8 induction by mechanical stresses, indicating that IL-1 beta is essential for IL-8 induction, presumably though autocrine or paracrine mechanisms. Finally, experiments with signal-specific inhibitors indicated that MAP kinase activation is essential for IL-8 induction.