Intracellular localization of Borrelia burgdorferi : implications for persistence, pathogenesis, and immune responsiveness of Lyme disease

The later stages of Lyme disease are characterized by persistence of Borrelia burgdorferi organisms in the presence of a strong anti-B. burgdorferi immune response. This suggests the B. burgdorferi may hide to avoid the defenses of the host or that there is a reservoir for the organisms in the host. In this thesis project, it has been demonstrated that B. burgdorferi gain entrance into human umbilical vein endothelial cells and murine endothelial cells. Incubation of two strains of B. burgdorferi with human and murine endothelial cells results in adhesion and invasion. The intracellular location of the spirochetes was demonstrated by the incorporation of 3H-adenine labeled B. burgdorferi into a trypsin-resistant compartment and was confirmed by double-immunofluorescence staining, which discriminates intracellular from extracellular organisms. Endothelia cell activation had not effect on the interaction of B burgdorferi with endothelia cells; however, B. burgdorferi infection did induce the endothelia cell product IL-6. As IL-6 is an important inflammatory mediator, it may be involved in the pathology of Lyme disease. Analysis of the antigen specific response of lymphocytes from infected animals allowed us to determine T cells were involved. The establishment of an animal model will allow further studies on the role of the host immune response in the pathology associated with B. burgdorferi infection.