| 引用本文： |
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谭正午,徐盼,郭艺婷,等.产黑普氏菌破坏上皮屏障紧密连接在口腔扁平苔藓发病机制中的作用[J].同济大学学报（医学版）,2021,42(4):459-466. [点击复制]
- TAN Zheng-wu,XU Pan,GUO Yi-ting,et al.Prevotella melaninogenica impairs oral epithelial barrier through inhibiting tight junction proteins as mechanism of pathogenesis of oral lichen planus[J].同济大学学报（医学版）,2021,42(4):459-466. [点击复制]
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| 摘要: |
| 目的探索产黑普氏菌（Prevotella melaninogenica， Pm）侵入口腔扁平苔藓（oral lichen planus， OLP）病损组织的可能机制。方法收集OLP患者病损组织和正常黏膜组织，应用免疫组织化学染色检测闭锁小带蛋白-1（zonula occludin-1， ZO-1）和连接黏附分子-1（junctional adhesion molecule-1， JAM-1）的表达。将Pm与人口腔角质形成细胞（human oral keratinocytes， HOK）共培养，通过Transwell小室实验检测荧光素异硫氰酸酯-葡聚糖4KD（FITC-dextran 4KD， FD4）的渗透量，观察Pm对HOK上皮屏障功能的影响，并采用qPCR检测ZO-1和JAM-1的表达改变。结果OLP患者病损组织中ZO-1、JAM-1的表达显著低于正常组织（P<0.01，P<0.0001）。FD4的渗透量随Pm浓度增加而增加（P<0.05）。Pm与HOK细胞共培养后，ZO-1、JAM-1表达均显著减少（P<0.005；P<0.05），并随着Pm浓度增加或时间延长而降低。结论Pm可能通过抑制紧密连接蛋白ZO-1、JAM-1的表达而破坏OLP上皮组织屏障，从而侵入上皮组织导致慢性炎症，在口腔扁平苔藓发生发展中起到重要作用。 |
| 关键词: 口腔扁平苔藓 产黑普氏菌 紧密连接蛋白 上皮屏障功能 |
| DOI：10.12289/j.issn.1008-0392.21048 |
| 投稿时间：2021-02-15 |
| 基金项目:国家自然科学基金（81870764） |
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| Prevotella melaninogenica impairs oral epithelial barrier through inhibiting tight junction proteins as mechanism of pathogenesis of oral lichen planus |
| TAN Zheng-wu,XU Pan,GUO Yi-ting,HE Yuan |
| (Dept. of Oral Medicine， School & Hospital of Stomatology， Tongji University, Shanghai Engineering Research Center of Tooth Restoration and Regeneration， Shanghai 200072， China) |
| Abstract: |
| ObjectiveTo explore the mechanism of Prevotella melaninogenica(Pm) in pathogenesis of oral lichen planus(OLP). MethodsThe expression of tight junction proteins zonula occludin-1(ZO-1) and junctional adhesion molecule-1(JAM-1) in OLP and normal mucosal samples was detected by immunocytochemistry(IHC). Pm and human oral keratinocytes(HOK) cells were co-cultured, the permeability of HOC cells was detected with Transwell assay using FITC-dextran 4KD(FD4) as an indicator; the mRNA expression of ZO-1 and JAM-1 was detected by qRT-PCR. ResultsThe expression of ZO-1 and JAM-1 in OLP samples was significantly lower than that in the normal tissue(P<0.01，P<0.0001). After co-culture of HOC cells with Pm, the permeability of FD4 was significantly increased in a concentration-dependent manner(P<0.05); and the expression of ZO-1 and JAM-1 mRNA was significantly decreased in a concentration-and time-dependent manner(P<0.005; P<0.05). ConclusionPm can disrupt OLP epithelial barrier by inhibiting the expression of tight junction proteins ZO-1 and JAM-1, leading to chronic inflammation, which may be the mechanism of OLP pathogenesis. |
| Key words: oral lichen planus Prevotella melaninogenica tight junction protein epithelial barrier function |
