Tp17 membrane protein of Treponema pallidum activates endothelial cells in vitro

• Treponema pallidum membrane protein Tp17 plays a role in inflammatory mediators during syphilis.
• The rTp17 protein may up-regulate expression of adhesion molecules on endothelial cells.
• The rTp17 protein also increased the transendothelial migration of monocytes.
• The ability of TP17 to activate endothelial cells may play an important role in the immunopathogenesis of syphilis.

Tp17, a membrane immunogen of Treponema pallidum subsp. pallidum, was initially recognized as an inflammatory mediator of syphilis. Because the histopathology of syphilis is characterized by endothelial cell abnormalities, we investigated the effects of recombinant Tp17 (rTp17) on endothelial cell activation in vitro. Using real-time reverse transcription-PCR and whole-cell ELISA, we found that rTp17 activated endothelial cells, as demonstrated by the up-regulated expression and increased gene transcription of intercellular adhesion molecule 1 (ICAM-1), E-selectin, and monocyte chemoattractant protein-1 (MCP-1). rTp17 also enhanced the migration and subsequent adhesion of monocytes to endothelial cells as well as increased transendothelial migration of monocytes. These data suggest that the ability of Tp17 to activate endothelial cells may play an important role in the immunopathogenesis of syphilis.