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A Novel In vitro Model for Studying the Interactions Between Human Whole Blood and Endothelium
Published on: November 21, 2014
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.
Abstract:
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.
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.
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