EXACERBATION OF LYME ARTHRITIS IN BEIGE MICE

Borrelia burgdorferi-induced disease susceptibility was explored in di sease-resistant C57/BL6 (B6) and -susceptible C3H/He (C3H) mice with a nd without the beige (bg) mutation, which is associated with granulocy te and NK cell dysfunction. Both B6 and C3H mice had more prevalent an d severe arthritis than their congenic partners, and B6-bg mice develo ped arthritis equal in severity to that in C3H mice. Spirochetes were visualized in joint tissue of B6-bg mice but not B6 mice. No differenc es in spirochete isolation from tissues or immunoglobulin titers to B. burgdorferi were noted between groups. Depletion of granulocytes with cyclophosphamide and macrophages with silica in B6 and C3H mice modif ied arthritis susceptibility, but depletion of NK cells by serotherapy in B6 mice had no effect on disease. This study demonstrates that inn ate genetic resistance to Lyme arthritis in mice can be overcome by a single gene mutation, which is probably mediated through granulocyte f unction.