Abstract
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.
Highlights
The endothelial barrier, constituted by the vascular endothelial cells lining the inner lumen of blood vessels and capillaries, plays a crucial role in the health and integrity of tissues by regulating the passage of molecules, liquids and immune cells [1, 2, 3]
In an in vitro static assay of transendothelial migration, we examined whether incubation of human umbilical vein endothelial cells (HUVECs) with recombinant Treponema pallidum protein Tp0965 (rTp0965) would result in an increased migration of monocytes across the monolayer
Previous studies demonstrated that T. pallidum and the T. pallidum 47 kDa antigen activated cultured human dermal microvascular endothelial cells (HDMECs) to up-regulate the expression of adhesion molecules in a concentration and time-dependent manner [20, 21]
Summary
The endothelial barrier, constituted by the vascular endothelial cells lining the inner lumen of blood vessels and capillaries, plays a crucial role in the health and integrity of tissues by regulating the passage of molecules, liquids and immune cells [1, 2, 3]. The rTp0965 Protein and Immunopathogenesis of Syphilis vascular endothelium [6, 7, 8] They can trigger the opening of the intercellular junction, induce apoptosis of endothelial cells or activate the immune system, which in turn leads to the destruction of the endothelial barrier and subsequent edema [9, 10, 11, 12]. Neisseria meningitides [13], as well as Staphylococcus aureus [14], adhere to endothelial cells, and induce the expression of endothelial adhesion molecules (ICAM-1, E-selectin, and VCAM-1), which contribute to leukocyte attachment. The outer surface lipoprotein A (OspA) of Borrelia burgdorferi, as shown with Neisseria meningitides, increases the expression of endothelial adhesion molecules (ICAM-1, E-selectin, and VCAM-1) of HUVECs and subsequently adds to the transendothelial migration of neutrophils in vitro [16]
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