The Effect of B. burgdorferi Infection on Cytokine Expression of the Mammalian Host

Abstract

Lyme disease, or Lyme borreliosis, is a multi-organ, zoonotic disease predominant in the northern hemisphere. Lyme borreliosis is caused by different members of the genus Borrelia, most notably Borrelia burgdorferi. The spirochete is transmitted to humans by a tick vector during its blood meal. Lyme disease results in a wide range of symptoms making the disease difficult to diagnose. These various clinical manifestations are due to the spirochetes’ ability to extravasate into different tissues all over the body. Previous studies have shown that treatment with IL-10, TNF-α, and MCP-1 can potentiate the vasculature and accelerate the vascular transmigration process. The direct assessment of cytokine transcript levels from mouse leukocytes that can contribute to extravasation had not previously been reported. In this study, we analyzed the effects of infection with various strains of B. burgdorferi at different time points before vascular transmigration on the cytokine transcript levels of host leukocytes. Additionally, we further characterized the differences between BALB/c and Cd1d -/- mice in their inflammatory responses.