Borrelia burgdorferi-induced oxidative burst, calcium mobilization, and phagocytosis of human neutrophils are complement dependent

When Borrelia burgdorferi, the spirochete causing Lyme disease, is transmitted to a human, the complement system is among the first challenges facing the bacterium. Neutrophils are crucial leukocytes in the first line of host defense against bacterial infections. To investigate the role of complement in the Borrelia-induced activation of human neutrophils, oxidative burst, calcium mobilization, and phagocytosis induced by three subspecies of B. burgdorferi were studied. Each subspecies induced all observed neutrophil functions in a complement-dependent manner. Serum-derived factors bound to the surface of B, burgdorferi were found to be essential for the induction of the oxidative burst. The CD11b chain of CR3 was found to participate in the oxidative burst and calcium mobilization induced by B. burgdorferi.