CCL20 production is induced in human dental pulp upon stimulation by Streptococcus mutans and proinflammatory cytokines
CCL20 production is induced in human dental pulp upon stimulation by Streptococcus mutans and proinflammatory cytokines
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DOI：
10.1111/j.1399-302x.2008.00431.x
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发表时间：
2008-08-01
影响因子：
--
通讯作者：
Matsuo, T.
中科院分区：
文献类型：
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作者：
Takahashi, K.;Nakanishi, T.;Matsuo, T.
简介：牙髓炎的特点是炎症细胞明显浸润，以响应龋相关细菌的入侵。众所周知，趋化因子调节淋巴细胞的运输，CC趋化因子配体20 （CCL20）最近被证明在募集记忆T细胞和未成熟树突状细胞进入炎性病变中发挥关键作用。我们之前报道CCL20主要表达于炎症牙髓组织中积聚的微血管内皮细胞和巨噬细胞中，其特异性受体CCR6在浸润淋巴细胞上表达。然而，CCL20的表达机制尚不清楚。方法与结果：在本研究中，我们研究了龋齿相关细菌代表变形链球菌或促炎细胞因子刺激后单核/巨噬细胞、内皮细胞和牙髓成纤维细胞中CCL20的表达。用逆转录聚合酶链反应在炎症牙髓中检测到CCL20信使RNA，而在临床正常牙髓中检测不到。通过酶联免疫吸附实验，S. mutans诱导人单核细胞系、分化的巨噬细胞样THP-1细胞和人脐静脉内皮细胞（HUVEC）产生增加的CCL20。变形链球菌的脂磷胆酸也能通过HUVEC诱导CCL20的产生。此外，白细胞介素-1 β和肿瘤坏死因子- α刺激可增加髓质成纤维细胞的CCL20生成。结论：CCL20的表达受龋相关细菌深入牙本质小管的刺激和牙髓病变的促炎细胞因子的诱导。它可能通过炎症细胞的积累参与牙髓炎的进展。
Introduction: Pulpitis is characterized by the marked infiltration of inflammatory cells in response to an invasion of caries-related bacteria. It is well known that chemokines regulate the trafficking of lymphocytes, and CC chemokine ligand 20 (CCL20) has been recently shown to play a crucial role in the recruitment of memory T cells and immature dendritic cells into inflammatory lesions. We previously reported that CCL20 was mainly expressed in microvascular endothelial cells and macrophages that accumulated in inflamed pulp tissues and that its specific receptor, CCR6, was expressed on infiltrated lymphocytes. However, the mechanism of CCL20 expression remains unclear.Methods and Results: In this study, we investigated the expression of CCL20 in monocytes/macrophages, endothelial cells, and pulpal fibroblasts after stimulation with Streptococcus mutans, a representative of caries-related bacteria, or proinflammatory cytokines. CCL20 messenger RNA was detected by reverse transcription-polymerase chain reaction in inflamed pulp, but not in clinically normal pulp. By enzyme-linked immunosorbent assay, S. mutans induced a human monocytic cell line, differentiated macrophage-like THP-1 cells, and human umbilical vein endothelial cells (HUVEC) to produce an increased amount of CCL20. Lipoteichoic acid from S. mutans also elicited CCL20 production by HUVEC. Moreover, CCL20 production from pulpal fibroblasts was increased by stimulation with inetrleukin-1 beta and tumor necrosis factor-alpha.Conclusion: Our results indicate that CCL20 expression is induced by stimulation with caries-related bacteria that have invaded deeply into the dentinal tubules as well as by proinflammatory cytokines in the inflamed pulpal lesions. It may be involved in the progression of pulpitis via accumulation of inflammatory cells.