Hosokawa Yoshitaka, Hosokawa Ikuko, Shindo Satoru, Ozaki Kazumi, Matsuo Takashi
Department of Conservative Dentistry, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15 Kuramoto-cho, Tokushima, Tokushima, 770-8504, Japan.
Department of Oral Health Care Promotion, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima, Tokushima, Japan.
Inflammation. 2015 Dec;38(6):2252-8. doi: 10.1007/s10753-015-0209-y.
Vitamin D has important roles on control of calcium and phosphate levels in the body. However, the role of vitamin D on the pathogenesis of periodontal disease is still uncertain. Therefore, we examined the effect of the hormonal form of vitamin D, calcitriol, on inflammatory responses of human periodontal ligament cells (HPDLC). We detected vitamin D receptor expression in non-stimulated HPDLC. Calcitriol inhibited interleukin (IL)-6, IL-8, CC chemokine ligand (CCL) 20, CXC chemokine ligand (CXCL) 10, and matrix metalloproteinase (MMP)-3 release from IL-1β-stimulated HPDLC. Tissue inhibitor of metalloproteinase (TIMP)-1 production did not change by calcitriol. Moreover, we found c-jun N-terminal kinase (JNK) phosphorylation and IκB-α degradation in IL-1β-stimulated HPDLC were inhibited by calcitriol, and JNK and nuclear factor (NF)-κB inhibitors could decrease IL-6, IL-8, CCL20, CXCL10, and MMP-3 productions in IL-1β-treated HPDLC. These findings suggest that vitamin D could modulate inflammatory response in periodontal tissues.
维生素D在控制人体钙和磷水平方面发挥着重要作用。然而,维生素D在牙周病发病机制中的作用仍不明确。因此,我们研究了维生素D的激素形式骨化三醇对人牙周膜细胞(HPDLC)炎症反应的影响。我们检测了未受刺激的HPDLC中维生素D受体的表达。骨化三醇抑制白细胞介素(IL)-6、IL-8、CC趋化因子配体(CCL)20、CXC趋化因子配体(CXCL)10以及基质金属蛋白酶(MMP)-3从IL-1β刺激的HPDLC中的释放。骨化三醇对金属蛋白酶组织抑制剂(TIMP)-1的产生没有影响。此外,我们发现骨化三醇抑制了IL-1β刺激的HPDLC中的c-jun氨基末端激酶(JNK)磷酸化和IκB-α降解,并且JNK和核因子(NF)-κB抑制剂可降低IL-1β处理的HPDLC中IL-6、IL-8、CCL20、CXCL10和MMP-3的产生。这些发现表明维生素D可以调节牙周组织中的炎症反应。