Study on the role of chemokines in the infiltration of inflammatory cells in dental pulp tissue destruction

趋化因子在牙髓组织破坏中炎症细胞浸润中的作用研究

• 批准号: 13672001
• 负责人: NAKANISHI Tadashi
• 金额: $ 2.24万
• 依托单位: The University of Tokushima
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2001
• 资助国家: 日本
• 起止时间: 2001 至 2002
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-13672001/
• 关键词: pulpitis; MIP-3α; CCR6; macrophage; endothelial cell; lymphocyte; chemokine; chemokine receptor; RT-PCR; ELISA; Streptococcus mutans; IL-1β; TNF-α; CD45RO; 免疫染色

Severe pulpitis resulted from dental caries is characterized by a marked inflammatory infiltrate such as lymphocytes. Little is known about the recruitment of these cells into the lesion of dental plup in carious teeth. Macrophage inflammatory protein-3α (MIP-3α), one of the CC chemokines, is known to attract CC chemokine receptor 6 (CCR6)-expressing T cells, and CCR6 is typically expressed on memory T cells.Then, we ezamined the expression of MIP-3α Mrna by RT-PCR and the distribution of MIP-3α-positive and CCR6-positive cells by immunohistochemistry in human dental pulp. MIP-3α expression was observed in all of the inflamed pulp samples, and microvascular endothelial cells. Moreover, CCR6 expression was also observed in the infiltrating lymphocytes, predominantly memory phenotype T cells. In contrast, MIP-3α and CCR6 was scarcely detected in normal pulps.We also examined the pattern of MIP-3α expression in endothelial cells stimulated by Streptococcus mutans or cytokine (IL-1 β or TNF α) in vitro. The level of MIP-3α increased in time- and dose-dependent manner, and that both cytokines strongly induced MIP-3α secretion compared with S. mutans.These findings suggest that MIP-3α plays an important role in the advancement of pulpal inflammation via the recruitment of CCR6-expressing lymphocytes. Furthermore, this study indicate that endothelial cells may modulate the accumulation of lymphocytes through the MIP-3α production.

由龋齿引起的严重牙髓炎的特征在于显著的炎性浸润，例如淋巴细胞。关于这些细胞在龋坏牙齿的牙髓损伤中的募集知之甚少。巨噬细胞炎性蛋白-3 α（macrophage inflammatory protein-3α，MIP-3α）是CC趋化因子之一，能吸引表达CC趋化因子受体6（CCR 6）的T细胞，CCR 6主要表达于记忆性T细胞。MIP-3α在所有炎症牙髓组织及微血管内皮细胞中均有表达。此外，在浸润淋巴细胞中也观察到CCR 6表达，主要是记忆表型T细胞。我们还检测了MIP-3 α在变形链球菌（Streptococcus mutans）和细胞因子（IL-1 β或TNF α）刺激的内皮细胞中的表达模式。与S.这些发现表明MIP-3α通过募集表达CCR 6的淋巴细胞在牙髓炎症的进展中起重要作用。此外，本研究还提示内皮细胞可能通过分泌MIP-3α来调节淋巴细胞的聚集。

项目成果

T.Nakanishi et al.: "Expression of macrophage inflammatory protein-3α in human pulpitis"Journal of Dental Research. 81(Special Issue). 44-44 (2002)

T. Nakanishi 等：“人牙髓炎中巨噬细胞炎症蛋白 3α 的表达”《牙科研究杂志》81（特刊）（2002 年）。

Y.Hosokawa et al.: "Macrophage inflammatory protein-3α-CC chemokine receptor 6 interactions play an important role in CD4+ T-cell accumulation in periodontal diseased tissue"Clinical and Experimental Immunology. 128. 548-554 (2002)

Y.Hosokawa 等人：“巨噬细胞炎症蛋白-3α-CC 趋化因子受体 6 相互作用在牙周病组织中 CD4+ T 细胞积累中发挥重要作用”《临床和实验免疫学》128. 548-554 (2002)。