Anti-tumor necrosis factor-alpha treatment activates Borrelia burgdorferi spirochetes 4 weeks after ceftriaxone treatment in C3H/He mice.

Background: The effect of anti-tumor necrosis factor (TNF)-alpha treatment in Borrelia burgdorferi-infected and ceftriaxone-treated C3H/He mice was evaluated.

Methods: Mice were infected with B. garinii A218 or B.

Persistent joint swelling and Borrelia-specific antibodies in Borrelia garinii-infected mice after eradication of vegetative spirochetes with antibiotic treatment.

We wanted to study the pathogenesis and the long-term manifestations of Borrelia garinii infection in SJL and C3H/He mice. We report here that B. garinii A218 causes a persisting infection in these mouse strains.

Sublethal concentrations of complement can effectively opsonize Borrelia burgdorferi.

The fate of borreliae invading a human may depend on the early innate response they induce. The interactions of human complement system and neutrophils with two strains of the Lyme borreliosis spirochete Borrelia burgdorferi were studied. Borrelia burgdorferi sensu stricto B31 (resistant to a 28% concentration of normal human serum (NHS)) and Borrelia garinii Bg A218/98 (sensitive to 7% NHS) were examined.

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.

Tube phagocytosis, a novel way for neutrophils to Phagocytize borrelia burgdorferi.

Interactions between human neutrophils and Borrelia burgdorferi, the Lyme disease spirochete, were studied by dark-field microscopy combined with video technology. A previously unrecognized mechanism for neutrophils to phagocytize the spirochete was discovered. During phagocytosis, the spirochete attaches to the neutrophil head-on, the neutrophil forms a thin tubelike protrusion around the bacterium, and the fully covered spirochete is drawn into the cell.