BORRELIA-BURGDORFERI OUTER SURFACE PROTEIN-A (OSPA) ACTIVATES AND PRIMES HUMAN NEUTROPHILS

Lyme disease is caused by infection with the spirochete Borrelia borgd orferi and is characterized by bacterial persistence and inflammation of many host tissues. B. burgdorferi express outer surface lipoprotein s, including OspA, with inflammatory properties that could contribute to the localized tissue inflammation. Neutrophils are the predominant infiltrate into the inflamed arthritic joints, and are crucial for con trolling the spirochete infection. They may also contribute to the joi nt pathology associated with Lyme arthritis. This study examines the e ffect of OspA on the activities of the neutrophil, Picomolar concentra tions of OspA induce surface markers associated with neutrophil activa tion: increased CD10 and CD11b expression; decreased CD62-L expression ; and an increased adherence to extracellular matrix. These events wer e similar in kinetics and magnitude to those induced by the strong act ivators LPS and FMLP. Like LPS, OspA could prime neutrophils for FMLP- induced release of lysosomal granules and production of superoxide. Th us, models of Lyme arthritis should include the possible contribution of direct activation of neutrophils to both defense and disease.