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Low-passage isolates of Borrelia burgdorferi induced arthritis when injected into the hind paws of irradiated hamsters, while high-passage isolates did not. To examine a possible mechanism for induction of arthritis, peritoneal exudate cells were coincubated with high- and low-passage isolates of B. burgdorferi, and the resultant conditioned medium was assayed for interleukin-1 (IL-1) activity. Comparable amounts of IL-1 activity were detected in culture supernatants generated by high- and low-passage spirochetes and were dependent on the number of spirochetes added. Live B. burgdorferi stimulated greater release of IL-1 activity than did heat-killed organisms. No evidence of release of IL-1 due to shedding of soluble components from spirochetes was obtained. A recombinant human IL-1 receptor antagonist blocked the proliferative activity of conditioned medium in a murine thymocyte assay for IL-1 activity. The greater ability of low-passage spirochetes to survive in vivo may be more important than the ability to induce IL-1 production in the pathogenesis of Lyme arthritis.

An in vitro borreliacidal assay that accurately reflects the levels of protective antibody determined by passive transfer of immunity studies was developed. Borreliacidal antibody in sera obtained from normal hamsters infected with Borrelia burgdorferi was readily detected. When immune serum containing complement was incubated with B. burgdorferi organisms, spirochetes were killed within 2 h. Treating immune serum with anti-hamster immunoglobulin G abrogated the borreliacidal activity. Killing of B. burgdorferi in serum was detected 1 week after infection; it peaked at week 3 and gradually declined. Relatively high levels of borreliacidal antibody were found, especially in week 3 immune serum, which could be diluted 1,280-fold. The decrease in borreliacidal antibody after infection may account for occurrences of reinfection and the remitting course of Lyme disease.