T. pallidum ; 47kDa antigen ; Human dermal microvascular endothelial cells ; Fibronectin ; Migration
Abstract
For T. pallidum to disseminate and cause systemic infection, it must traverse the endothelial cells lining the vasculature. In inflammatory and immune reactions, vascular endothelial cells act as key effectors. Fibronection appears to be important to T. pallidum cytadherence, because antifibronectin antibody prevents attachment of the T. pallidum to host cells and fibronectin-coated glass surfaces. We investigated the binding assay of T. pallidum to cultured human dermal microvascular endothelial cells (HDMEC) or fibronectin.
We observed the adherence of T. pallidum to HDMEC and small percentage of adherent T. pallidum traverse through HDMEC monolayer, but the nonpathogenic treponemes and heat-inactivated T. pallidum failed to bind and trasverse to HDMEC. The adherence of T. pallidum to HDMEC was increased by a 47kDa antigen of T. pallidum of TNF-α. We also observed the adherence of T. pallidum to fibronectin. These findings suggest that only live pathogenic T. pallidum is capable of binds to HDMEC or fibronection and the binding of T. pallidum to HDMEC can be regulated by a 47kDa antigen of T. pallidum.