DbpA is a target for
antibodies that protect mice against
infection by cultured Borrelia burgdorferi. Infected mice exhibit early and sustained humoral responses to
DbpA and DbpB, suggesting that these
proteins are expressed in vivo. Many
antigens expressed in mammals by B. burgdorferi are repressed in vitro at lower growth temperatures, and we have now extended these observations to include
DbpA and DbpB. To confirm that the protective
antigen DbpA is expressed in vivo and to address the question of its accessibility to
antibodies during
infection, we examined B. burgdorferi in blood samples from mice following cutaneous inoculation. B. burgdorferi was visualized by dark-field microscopy in plasma samples from spirochetemic mice, and an indirect immunofluorescence assay showed that these spirochetes were
DbpA positive and OspA negative. We developed an ex vivo borreliacidal assay to show that hyperimmune antiserum against
DbpA, but not OspA, killed these plasma-derived spirochetes, demonstrating that
DbpA is accessible to
antibodies during this phase of
infection. Blood transferred from spirochetemic donor mice readily established B. burgdorferi
infection in naive recipient mice or mice hyperimmunized with OspA, while mice hyperimmunized with
DbpA showed significant protection against challenge with host-adapted spirochetes. Antiserum from persistently infected mice had borreliacidal activity against both cultured and plasma-derived spirochetes, and adsorption of this serum with
DbpA substantially depleted this killing activity. Our observations show that immunization with
DbpA blocks B. burgdorferi dissemination from the site of cutaneous inoculation and suggest that
DbpA antibodies may contribute to control of
persistent infection.