Tumor Necrosis Factor Receptor-associated Factor 6 Plays a Role in the Inflammatory Responses of Human Periodontal Ligament Fibroblasts to Enterococcus faecalis
Tumor Necrosis Factor Receptor-associated Factor 6 Plays a Role in the Inflammatory Responses of Human Periodontal Ligament Fibroblasts to Enterococcus faecalis
复制标题
肿瘤坏死因子受体相关因子6在人牙周膜成纤维细胞对粪肠球菌的炎症反应中发挥作用
DOI：
10.1016/j.joen.2015.08.028
复制
发表时间：
2015-12-01
影响因子：
4.2
通讯作者：
Huang, Dingming
中科院分区：
文献类型：
--
作者：
Zhang, Lan;Wang, Tingting;Huang, Dingming
前言：粪肠球菌是一种常见于根尖周病损或继发感染的微生物。然而，没有证据表明E.粪便直接在根尖区引起炎症。本研究旨在探讨人牙周膜成纤维细胞（PDLs）对E。粪便。方法：用热灭活的E. faecalis（HKEF）或来自E.粪肠球菌（LTA），有或没有沉默肿瘤坏死因子受体相关因子6（TRAF 6）。采用实时定量聚合酶链反应和Western blot检测Toll样受体2/4、核苷酸结合寡聚化结构域1/2和TRAF 6的表达。用酶联免疫吸附试验测定细胞上清液中促炎细胞因子的分泌，包括白细胞介素-1 β、白细胞介素-6、白细胞介素-8和肿瘤坏死因子-α。结果：HKEF和LTA均能刺激Toll样受体2和TRAF 6的表达，且呈时间依赖性。促炎细胞因子的分泌也增加。在沉默TRAF 6后，由HKEF或LTA诱导的促炎细胞因子的上调减弱。结论：TRAF 6在大肠杆菌致炎过程中起重要作用。faecalis或其在PDL中的LTA。
Introduction: Enterococcus faecalis is a frequently isolated microorganism in persistent periapical lesion or secondary infection. However, no evidence has demonstrated that E. faecalis induced inflammation directly in the apical area. This study aimed to explore the mechanism of the inflammatory responses of human periodontal ligament fibroblasts (PDLs) to E. faecalis. Methods: PDLs were stimulated with heat-killed E. faecalis (HKEF) or lipoteichoic acid from E. faecalis (LTA) with or without silencing of tumor necrosis factor receptor-associated factor 6 (TRAF6). The expressions of toll-like receptor 2/4, nucleotide-binding oligomerization domain 1/2, and TRAF6 were detected by using quantitative real-time polymerase chain reaction and Western blot. The secretions of proinflammatory cytokines, including interleukin-1 beta, interleukin-6, interleukin-8, and tumor necrosis factor-alpha, were determined in the cell supernatants with enzyme-linked immunosorbent assay. Results: Both HKEF and LTA stimulated the expression of toll-like receptor 2 and TRAF6 in a time-dependent manner. The secretions of proinflammatory cytokines were also increased. After silencing TRAF6, the upregulations of proinflammatory cytokines induced by HKEF or LTA were attenuated. Conclusions: TRAF6 plays a pivotal role in inflammation induced by E. faecalis or its LTA in PDLs.