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Recombinant Treponema pallidum Protein Tp0965 Activates Endothelial Cells and Increases the Permeability of Endothelial Cell Monolayer

机译:重组梅毒螺旋体蛋白Tp0965激活内皮细胞并增加内皮细胞单层的通透性

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摘要

The recombinant Treponema pallidum protein Tp0965 (rTp0965), one of the many proteins derived from the genome of T. pallidum subsp. pallidum, shows strong immunogenicity and immunoreactivity. In this study, we investigated the effects of rTp0965 on the endothelial barrier. Treatment of human umbilical vein endothelial cells (HUVECs) with rTp0965 resulted in increased levels of ICAM-1, E-selectin, and MCP-1 mRNA and protein expression. These increases contributed to the adhesion and chemataxis of monocytes (THP-1 cells) to HUVECs preincubated with rTp0965. In addition, rTp0965 induced reorganization of F-actin and decreased expression of claudin-1 in HUVECs. Interestingly, inhibition of the RhoA/ROCK signal pathway protected against rTp0965-induced higher endothelial permeability as well as transendothelial migration of monocytes. These data indicate that Tp0965 protein may play an important role in the immunopathogenesis of syphilis.
机译:重组梅毒螺旋体蛋白Tp0965(rTp0965),是从梅毒螺旋体亚种基因组衍生的许多蛋白之一。苍白,具有很强的免疫原性和免疫反应性。在这项研究中,我们调查了rTp0965对内皮屏障的影响。用rTp0965处理人脐静脉内皮细胞(HUVEC)导致ICAM-1,E-选择素和MCP-1 mRNA和蛋白表达水平升高。这些增加有助于单核细胞(THP-1细胞)与用rTp0965预孵育的HUVEC的粘附和化学趋化。此外,rTp0965诱导HUVEC中F-肌动蛋白的重组并降低claudin-1的表达。有趣的是,对RhoA / ROCK信号通路的抑制可防止rTp0965-诱导的较高的内皮通透性以及单核细胞的跨内皮迁移。这些数据表明Tp0965蛋白可能在梅毒的免疫发病机制中起重要作用。

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