Plasminogen activator inhibitor-1 (PAI-1) is associated with nonalcoholic fatty liver disease (NAFLD) by lipid accumulation in the liver. In this study, we showed that extracellular vesicles (EVs) from the periodontal pathogens Filifactor alocis and Porphyromonas gingivalis induced steatosis by inducing PAI-1 in the liver and serum of mice fed a low-fat diet. PAI-1 induction was not observed in TLR2^−/− mice. When tested using HEK-Blue hTLR2 cells, human TLR2 reporter cells, the TLR2-activating ability of serum from NAFLD patients (n = 100) was significantly higher than that of serum from healthy subjects (n = 100). Correlation analysis confirmed that PAI-1 levels were positively correlated with the TLR2-activating ability of serum from NAFLD patients and healthy subjects. Amphiphilic molecules in EVs were involved in PAI-1 induction. Our data demonstrate that the TLR2/PAI-1 axis is important for hepatic steatosis by EVs of periodontal pathogens.

中文翻译：

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牙周病原体的细胞外囊泡通过 Toll 样受体 2 和纤溶酶原激活剂抑制剂 1 调节肝脂肪变性

纤溶酶原激活剂抑制剂-1 (PAI-1) 通过肝脏中的脂质积累与非酒精性脂肪肝 (NAFLD) 相关。在这项研究中，我们发现来自牙周病原体Filifactor alocis和牙龈卟啉单胞菌的细胞外囊泡 (EV)通过诱导低脂饮食小鼠肝脏和血清中的 PAI-1 来诱导脂肪变性。^{在 TLR2 −/−}小鼠中未观察到 PAI-1 诱导。当使用 HEK-Blue hTLR2 细胞（人 TLR2 报告细胞）进行测试时，NAFLD 患者血清 ( n = 100)的 TLR2 激活能力 显着高于健康受试者血清 ( n  = 100)。相关分析证实，NAFLD患者和健康受试者血清中PAI-1水平与TLR2激活能力呈正相关。EV 中的两亲分子参与 PAI-1 诱导。我们的数据表明，TLR2/PAI-1 轴对于牙周病原体 EV 引起的肝脂肪变性很重要。