Lyme disease, inflammation and autoimmunity
PhD, Microbiology and Immunology, University of Utah, Salt Lake City, UT, 2014
Lyme disease, caused by infection with the tick-borne pathogen Borrelia burgdorferi, is the most common vector-borne disease in the U.S., and is reaching epidemic levels in many regions, including the Upper Midwest. Lyme disease is an infection-induced multisystem disorder affecting skin (erythema migrans), heart (carditis), joints (arthritis) or neurologic tissue (neuroborreliosis) (Fig. 1). Although most patients are effectively treated with antibiotics, 10-20% of treated patients develop post-treatment Lyme disease syndromes, potentially resulting in months or years of disability. Identifying immune factors that contribute to variability in disease severity and treatment outcome is critically important for public health in Lyme-endemic communities such as Wisconsin.
Our basic research project focuses on elucidating cellular mechanisms of murine Lyme arthritis and Lyme carditis pathogenesis. Whereas some strains of mice appropriately regulate this inflammatory response to B. burgdorferi and develop mild disease, others fail to appropriately regulate immune responses and develop severe Lyme arthritis or Lyme carditis. We use this animal system as a model of infection-induced immune dysregulation by comparing strains of mice with different disease outcomes to effectively elucidate mechanisms Lyme disease pathogenesis in ways not possible in human patients.
Our translational research project involves working with clinicians to collect and analyze samples from patients with Lyme disease and other related inflammatory diseases here in Wisconsin. Many autoimmune and clinical features of post-infectious Lyme arthritis, the most common post-treatment syndrome, are similar to that seen in rheumatoid arthritis (Fig. 2), an autoimmune joint disease that may be triggered by oral or gut microbial infections. By using Lyme disease as a model of infection-induced autoimmunity, we may gain valuable insight into mechanisms of how infections may contribute to development of other autoimmune joint diseases.
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