Porphyromonas gingivalis lipopolysaccharide induces over production of CC chemokine ligand 2 via toll-like receptor-4 in oral lichen planus
Porphyromonas gingivalis lipopolysaccharide induces over production of CC chemokine ligand 2 via toll-like receptor-4 in oral lichen planus
复制标题
牙龈卟啉单胞菌脂多糖通过 Toll 样受体 4 诱导口腔扁平苔藓中 CC 趋化因子配体 2 的过量产生
DOI：
10.1111/jop.12655
复制
发表时间：
2018
影响因子：
3.3
通讯作者：
Tao Xiaoan
中科院分区：
文献类型：
--
作者：
Zeng Qi;Yang Xi;Chen Xiaobing;Xia Juan;Cheng Bin;Tao Xiaoan
背景我们最近报道CC趋化因子配体2（CCL 2）-CC受体2（CCR 2）轴参与口腔扁平苔藓（OLP）的发病机制。然而，CCL 2在OLP标本中高表达的确切机制尚不清楚。因此，本研究旨在探讨Toll样受体4（TLR-4）通路在OLP病变中CCL 2过度表达中的潜在作用。方法采用免疫组织化学染色和真实的实时RT-PCR检测TLR-4、CCL 2和CCR 2在OLP病变中的表达。然后，从OLP病变牙龈上皮细胞建立和牙龈卟啉单胞菌（P. gingivalis）脂多糖（LPS）处理。通过蛋白质印迹和真实的实时RT-PCR测定上皮细胞中的CCL 2表达。在一些实验中，TAK-242，TLR-4的特异性抑制剂，被用来阻断TLR-4通路之前，细胞用LPS.ResultsWe刺激发现，TLR-4是显着增加的上皮OLP标本，与对照组相比。LPS可诱导OLP上皮细胞产生CCL 2。TAK-242通过阻断TLR-4/NF-κB通路有效消除了LPS诱导的CCL 2表达增加。结论TLR-4在口腔扁平苔藓病变组织中表达增加，导致口腔扁平苔藓上皮中CCL 2表达上调，提示口腔细菌通过TLR-4途径参与了口腔扁平苔藓的发病过程。
BackgroundWe recently reported that the CC chemokine ligand 2 (CCL2)‐CC receptor 2 (CCR2) axis was involved in the pathogenesis of oral lichen planus (OLP). However, the exact mechanism for the high expression of CCL2 in OLP specimens is not clear. Therefore, this study was designed to investigate the potential role of the toll‐like receptor 4 (TLR‐4) pathway in overproduction of CCL2 in OLP lesions.MethodsImmunohistochemical staining and real‐time RT‐PCR were used to detect TLR‐4, CCL2, and CCR2 expression in OLP lesions. Then, gingival epithelial cells from OLP lesions were established and treated withPorphyromonas gingivalis(P. gingivalis)lipopolysaccharide (LPS). CCL2 expression in epithelial cells was determined by Western blotting and real‐time RT‐PCR. In some experiments, TAK‐242, a specific inhibitor of TLR‐4, was used to block the TLR‐4 pathway before cells were stimulated with LPS.ResultsWe found that TLR‐4 was significantly increased in the epithelium of OLP specimens, compared with controls. Moreover, LPS can induce the over production of CCL2 in epithelial cells of OLP, in vitro. TAK‐242 effectively eliminated the increase in CCL2 expression induced by LPS by blocking the TLR‐4/NF‐κB pathway. In addition, we again confirmed that expression of CCL2 and CCR2 was increased in OLP specimens.ConclusionIncreased TLR‐4 expression contributes to the upregulated expression of CCL2 in the epithelium of OLP lesions, which suggests that oral bacteria participate in the pathogenesis of OLP via the TLR‐4 pathway.