Jemiina Salo1, Annukka Pietikäinen1, Mirva Söderström2, Kaisa Auvinen3, Marko Salmi3, Rhodaba Ebady4, Tara J Moriarty4, Matti K Viljanen5, Jukka Hytönen5. 1. Department of Medical Microbiology and Immunology Turku Doctoral Program for Molecular Medicine. 2. Department of Pathology and Forensic Medicine, Turku University Hospital and University of Turku, Finland. 3. Department of Medical Microbiology and Immunology MediCity Research Laboratory, University of Turku. 4. Matrix Dynamics Group, Faculty of Dentistry Department of Laboratory Medicine and Pathobiology, Faculty of Medicine, University of Toronto, Canada. 5. Department of Medical Microbiology and Immunology.
Abstract
BACKGROUND: Bacterial pathogens causing systemic infections disseminate from the initial infection focus to the target organs usually through the blood vasculature. To be able to colonize various organs, bacteria need to adhere to the endothelial cells of the vascular wall, and the adhesion must be strong enough to resist the shear force of the blood flow.Borrelia burgdorferi sensu lato spirochetes, the causative agents of the tick-borne disease Lyme borreliosis, disseminate hematogenously from the tick bite site to the joints, the heart, and the central nervous system of the patient. METHODS: We used both wild-type and genetically modified B. burgdorferi s. l. bacteria, recombinant borrelia adhesins, and an array of adhesion assays carried out both under stationary and flow conditions to investigate the molecular mechanisms of borrelial adhesion to human endothelial cells. RESULTS: Borrelia garinii, a member of the B. burgdorferi s. l. complex, adhered to biglycan expressed by human endothelial cells in a flow-tolerant manner. The adhesion was mediated by the decorin-binding protein A (DbpA) and DbpB surface molecules of B. garinii. CONCLUSIONS: The proteoglycan biglycan is a receptor molecule for flow-resistant adhesion of the bacterial pathogen B. garinii on human endothelial cells.
BACKGROUND: Bacterial pathogens causing systemic infections disseminate from the initial infection focus to the target organs usually through the blood vasculature. To be able to colonize various organs, bacteria need to adhere to the endothelial cells of the vascular wall, and the adhesion must be strong enough to resist the shear force of the blood flow.Borrelia burgdorferi sensu lato spirochetes, the causative agents of the tick-borne disease Lyme borreliosis, disseminate hematogenously from the tick bite site to the joints, the heart, and the central nervous system of the patient. METHODS: We used both wild-type and genetically modified B. burgdorferi s. l. bacteria, recombinant borrelia adhesins, and an array of adhesion assays carried out both under stationary and flow conditions to investigate the molecular mechanisms of borrelial adhesion to human endothelial cells. RESULTS:Borrelia garinii, a member of the B. burgdorferi s. l. complex, adhered to biglycan expressed by human endothelial cells in a flow-tolerant manner. The adhesion was mediated by the decorin-binding protein A (DbpA) and DbpB surface molecules of B. garinii. CONCLUSIONS: The proteoglycan biglycan is a receptor molecule for flow-resistant adhesion of the bacterial pathogen B. garinii on human endothelial cells.
Authors: Berenice Plasencia-Muñoz; Francisco J Avelar-González; Mireya De la Garza; Mario Jacques; Adriana Moreno-Flores; Alma L Guerrero-Barrera Journal: Front Vet Sci Date: 2020-10-29