最近的研究表明外泌体与血管损伤有关。本研究探讨了梅毒螺旋体（T. pallidum）产生的树突状细胞衍生的外泌体对血管细胞炎症过程的影响。将人脐静脉内皮细胞 (HUVEC) 与从梅毒螺旋体诱导的树突状细胞中分离的外泌体共培养。使用蛋白质印迹和逆转录定量实时聚合酶链反应来评估 Toll 样受体 4 (TLR4) 的表达和促炎细胞因子的数量。研究结果表明，TLR4 的表达显着上调，并且 TLR4 敲低显着降低了外泌体中白细胞介素 1β (IL-1β)、白细胞介素 6 (IL-6) 和肿瘤坏死因子 α (TNF-α) 的产生。处理过的 HUVEC。此外，在外泌体处理的 HUVEC 中，TLR4 沉默降低了骨髓分化初级反应蛋白 88 (MyD88) 和活化 B 细胞核因子 kappa 轻链增强子 (NF-κB) 的水平。此外，用 NF-κB 抑制剂 BAY11-7082 抑制 NF-κB 的活性，也可以减少外泌体处理的炎症反应。我们的结果表明，梅毒螺旋体刺激的树突状细胞来源的外泌体诱导内皮细胞炎症，并且TLR4/MyD88/NF-κB信号轴被激活，显着增加IL-1β、IL-6和TNF-α的表达。这可能在梅毒的血管炎症反应中发挥重要作用，这将有助于了解梅毒的发病机制和宿主对梅毒螺旋体的免疫反应。

Exosomes have been implicated in vascular damage in recent research. The influence of dendritic cell-derived exosomes generated by Treponema pallidum (T. pallidum) on the inflammatory process of vascular cells was examined in this study. Human umbilical vein endothelial cells (HUVECs) were cocultured with exosomes isolated from dendritic cells induced by T. pallidum. Western blot and reverse transcription-quantitative real-time polymerase chain reaction were used to assess toll-like receptor 4 (TLR4) expression and the quantity of proinflammatory cytokines. The findings showed that the expression of TLR4 was considerably upregulated, and TLR4 knockdown dramatically reduced interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) production in exosome-treated HUVECs. Furthermore, TLR4 silencing reduced myeloid differentiation primary response protein 88 (MyD88) and nuclear factor kappa light chain enhancer of activated B cells (NF-κB) levels in exosome-treated HUVECs. Additionally, suppression of the activity of NF-κB with BAY11-7082, an NF-κB inhibitor, also reduced the exosome-treated inflammatory response. Our results suggested that dendritic cell-derived exosomes stimulated by T. pallidum induced endothelial cell inflammation, and the TLR4/MyD88/NF-κB signal axis was activated, significantly increasing IL-1β, IL-6, and TNF-α expression. This may have a significant role in the vascular inflammatory response in syphilis, which would contribute to the understanding of the pathogenesis of syphilis and the host immunological response to T. pallidum.