An in vivo induced membrane antigen of Lyme disease pathogen triggers murine joint inflammation (P6258)

Abstract

Abstract Borrelia burgdorferi bba57 is a plasmid-encoded gene-product of unknown function. Here we show that bba57 is induced in vivo and facilitates early murine infection. While BBA57 is not required for pathogen persistence during later phases of infection, unlike wild type isolate, the mutants failed to induce severe disease. We show that BBA57 is an outer membrane and surface-exposed antigen that is essential for the genesis of murine joint inflammation. Using a PCR array, we further identified that deficiency of BBA57 reduces the expression of selected “neutrophil-recruiting” chemokines and associated receptors in the joints that ultimately results in severe impairment of neutrophil infiltration. Similarly, using an established chemotaxis assay we demonstrated that BBA57 is directly involved in neutrophil migration in vitro. Taken together, our data suggest that BBA57 is a major trigger of murine Lyme arthritis, and that interfering with BBA57 may contribute to the development of new therapeutic strategy to prevent Lyme arthritis.