Endothelium damage caused by Treponema pallidum is the key step in the systemic dissemination and pathophysiology of syphilis, particularly cardiovascular syphilis and neurosyphilis. However, the molecular mechanisms supporting endothelium damage of syphilis are undefined. The outer membrane proteins were thought to be involved. Tp92 was first identified as an outer membrane protein of T. pallidum. Homologous proteins to Tp92 play important roles in cell attachment, inflammation, and tissue destruction in other bacterial species. In this study, we investigated the effect of Tp92 on endothelial cells activation. The data showed that Tp92 induced chemerin production in activated endothelial cells. Endothelial cell-derived chemerin upregulated the expression of TNF-α and ICAM-1 in endothelial cells via CMKLR1. In addition, endothelial cell-derived chemerin promoted THP-1-derived macrophage migration towards endothelial cells. These findings suggest that Tp92 may play an important role in mediating endothelial cell activation by inducing the secretion of chemerin.

梅毒螺旋体引起的内皮损伤是梅毒，尤其是心血管梅毒和神经梅毒的全身传播和病理生理学的关键步骤。但是，尚不清楚支持梅毒的内皮损伤的分子机制。外膜蛋白被认为参与其中。Tp92首先被鉴定为苍白螺旋体的外膜蛋白。Tp92的同源蛋白在其他细菌物种的细胞附着，炎症和组织破坏中起重要作用。在这项研究中，我们调查了Tp92对内皮细胞激活的影响。数据显示，Tp92诱导活化的内皮细胞产生凯莫瑞。内皮细胞来源的凯莫瑞通过CMKLR1上调了内皮细胞中TNF-α和ICAM-1的表达。另外，内皮细胞来源的凯莫瑞促进了THP-1来源的巨噬细胞向内皮细胞的迁移。这些发现表明，Tp92可能通过诱导chemerin的分泌在介导内皮细胞活化中起重要作用。