pallidum was found to localize to intercellular junctions. pallidum, disrupts the architecture of VE-cadherin, the main endothelial junctional protein which plays a key role in regulating vascular permeability. pallidum vascular adhesin Tp0751, as well as live T. Immunofluorescence microscopy demonstrated that a recombinant version of the only identified T. pallidum may be able to use both a paracellular route and a transcellular route for T. pallidum interacting with brain microvascular endothelial cells reveals that treponemes can merge with endothelial membranes ( Wu et al., 2017). Conversely, scanning electron microscopic imaging of T. pallidum interactions with aortic endothelial cells demonstrates that treponemes localize to intercellular junctions and traverse monolayers without disrupting barrier integrity ( Thomas et al., 1988). pallidum transendothelial migration are poorly understood. pallidum can invade diverse anatomical sites within the host, the molecular mechanisms that underlie the process of T. There are two recognized routes for transendothelial migration: transcellular traversal in which cells and pathogens induce endocytosis to cross the barrier, and paracellular traversal whereby cells and pathogens move in between cells at the sites of cellular junctions to access extravascular areas ( Lemichez et al., 2010). Bacterial pathogens that undergo systemic dissemination to invade secondary infection sites traverse the vascular endothelium to gain access to underlying tissue sites. Endothelial barriers play critical roles in regulating vascular hemostasis as well as innate and adaptive intravascular immune reactions in response to signals of inflammation, damage, or infection. The vascular endothelium is a dynamic cellular barrier that lines the luminal surfaces of blood vessels and separates the circulatory system from surrounding extravascular tissue and organ sites. pallidum can penetrate endothelial cell monolayers ( Riviere et al., 1989 Thomas et al., 1989). pallidum enters the bloodstream within hours of infection ( Raiziss and Severac, 1937 Cumberland and Turner, 1949) and that T. Treponema pallidum subspecies pallidum, the causative agent of syphilis, is a highly invasive pathogen that crosses the placental, blood-brain, and endothelial barriers. Further, treponemal localization to, and disruption of, intercellular junctions suggests that a paracellular route may also be utilized, a dual traversal strategy that has also been observed to occur for leukocytes and other invasive bacteria. pallidum can use a cholesterol-dependent, lipid raft-mediated endocytosis mechanism to traverse endothelial barriers. Collectively, these results suggest that T. pallidum is reduced by pretreatment of endothelial cells with filipin, an inhibitor that blocks cholesterol-mediated endocytosis. pallidum traverses endothelial barriers with no disruption in barrier permeability. Intriguingly, in this study we show that T. pallidum vascular adhesin (Tp0751), disrupts the architecture of the main endothelial junctional protein VE-cadherin. pallidum localizes to intercellular junctions and that viable T. Immunofluorescence microscopy reveals that a subpopulation of T. pallidum traversal of endothelial barriers. Herein, we investigate the mechanisms associated with T. Treponema pallidum subspecies pallidum, the causative agent of syphilis, traverses the vascular endothelium to gain access to underlying tissue sites. 3Department of Medicine, Division of Allergy and Infectious Diseases, University of Washington, Seattle, WA, United States.2Division of Medical Sciences, University of Victoria, Victoria, BC, Canada.1Department of Biochemistry and Microbiology, University of Victoria, Victoria, BC, Canada.Lithgow 1†, Emily Tsao 1, Ethan Schovanek 1, Alloysius Gomez 1, Leigh Anne Swayne 2 and Caroline E.
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