Complement-mediated killing of the Lyme disease spirochete Borrelia burgdorferi. Role of antibody in formation of an effective membrane attack complex.

摘要: Lyme disease is a multisystemic illness caused by the spirochete Borrelia burgdorferi. In absence of specific antibody, resistant to bactericidal activity C, despite capacity B. burgdorferi activate both C pathways. We examined mechanism serum resistance measuring deposition C3 and terminal components on in presence immune IgG. normal human antibody-sensitized borreliae bound similar amounts C3, or increased C8 C9, comparison unsensitized bacteria. However, at comparable levels C8, C9 uptake, only sensitized bacteria were killed. The requirement antibody for killing could not be explained differences rate ratio membrane attack complex (MAC). found that incubated C5-depleted serum, but C6-depleted killed when this treatment was followed missing components. Bacteria also reactive lysis (C5b-9) provided present. Therefore, effect IgG occurred stage C5b binding bacterial surface. Elution studies indicated MAC stably outer burgdorferi, whether treated with antibody. 0.1% trypsin released 48% 125I-C9 from surface 24% IgG-sensitized cells, demonstrating changed accessibility MAC. These results indicate process enhance extent initial component binding, rather alter allow effective formation.