Murine lyme disease: No evidence for active immune down-regulation in resolving or subclinical infection

Macrophages in vitro rapidly ingest and kill Borrelia burgdorferi, yet some spirochetes in vivo may survive in the host and lead to complications of L yme disease. One strategy for such survival may be the down-regulation of t he immune system. To test this, we evaluated the degree of macrophage activ ation in a site of active disease-the heart-by examining cytokine expressio n in murine macrophages from control and B. burgdorferi-infected animals. U sing double-label immunofluorescent staining in situ, we showed that infilt rating macrophages in infected hearts produce interleukin (IL)-1. By semiqu antitative reverse transcription- polymerase chain reaction analysis, incre ased levels of mRNA were measured for the proinflammatory cytokines IL-1, t umor necrosis factor-alpha, and IL-12 during peak and resolving disease. No increases in the anti-inflammatory cytokines IL-10 and transforming growth factor-beta were detected. In an infected site without active disease-the peritoneal cavity-no increases in levels of proinflammatory or anti-inflamm atory cytokines were detected in local macrophages. Thus, there is no evide nce of pressure toward the down-regulation of inflammatory activity in the regions tested.