Tp17 membrane protein of Treponema pallidum activates endothelial cells in vitro

Rui-Li Zhang1, Qian-Qiu Wang2, Jing-Ping Zhang2

  • 1Department of Dermatology, Wuxi Second Affiliated Hospital of Nanjing Medical University, Wuxi, Jiangsu Province, China.

Insights

The syphilis bacterium

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Syphilis, caused by Treponema pallidum subsp. pallidum, is characterized by endothelial cell abnormalities.
  • Tp17, a Treponema pallidum membrane immunogen, was previously identified as an inflammatory mediator.

Purpose of the Study:

  • To investigate the effects of recombinant Tp17 (rTp17) on endothelial cell activation in vitro.
  • To elucidate the role of Tp17 in the immunopathogenesis of syphilis.

Main Methods:

  • Real-time reverse transcription-PCR to assess gene transcription.
  • Whole-cell ELISA to measure protein expression.
  • In vitro assays to evaluate monocyte migration and adhesion to endothelial cells.

Main Results:

  • Recombinant Tp17 (rTp17) significantly activated endothelial cells.
  • rTp17 up-regulated the expression and gene transcription of intercellular adhesion molecule 1 (ICAM-1), E-selectin, and monocyte chemoattractant protein-1 (MCP-1).
  • rTp17 enhanced monocyte migration, adhesion to endothelial cells, and transendothelial migration.

Conclusions:

  • Tp17 activates endothelial cells, contributing to the inflammatory response in syphilis.
  • Endothelial cell activation by Tp17 may play a crucial role in the immunopathogenesis of syphilis.