Role of the apr lipoprotein in the pathogenesis of B. burgdorferi during murine infection
MetadataShow full item record
Infection with the bacterial agent of Lyme disease, Borrelia burgdorferi (Bb), results in a severely debilitating disease with clinical manifestations including arthritis, neurological impairment and cardiac inflammation.(1) Lyme arthritis associated with Bb infection occurs in a substantial number of untreated animal and human patients that can range in disease from mild to severe(2, 3). Important in Lyme disease pathology is the broad number of surface lipoproteins that can trigger host inflammatory responses.(4) Arp is one such surface lipoprotein that is upregulated during host infection and is encoded on the linear plasmid 28-1 (lp28-1) (5-7). While the function of this gene is unknown, anti-Arp antibody has been shown to reduce severity of arthritis in immunodeficient mice suggesting a role for this lipoprotein in inflammation (5, 6). Moreover a Bb strain lacking lp28-1 displayed reduced arthritis levels during murine infection (4, 7). Despite this evidence for a potential role in joint inflammation, direct mutational analysis of the arp gene has not been carried out to date. In this study, we demonstrate that a targeted deletion mutant of arp produces an intermediate level of joint arthritis in mice compared to the wild-type control. Future work should provide details on the exact timeline for the role of Arp in inflammation during infection, as well identifying any additional lp28-1-resident genes having a role in Lyme arthritis. Identifying factors involved in Bb pathogenesis and colonization of host joints is important as it may provide new targets for therapeutic intervention.