Hypercholesterolemia enhances early dissemination and Borrelia burgdorferi burden in a mouse model.

The Lyme disease spirochete, Borrelia burgdorferi, requires cholesterol to grow. The spirochete acquires cholesterol from the host to form cholesterol glycolipids, which are then incorporated into the spirochete's membrane. This study aimed to determine whether higher levels of serum cholesterol could facilitate the infection and contribute to the pathogenesis of Lyme disease. We investigated the effect of acute and chronic hypercholesterolemia on spirochetal infection in C3H/HeJ mice fed a high-fat diet (HF) compared to mice fed a control diet. The course of infection in mice was followed for 3 weeks (short-term effects) and 16 weeks post-infection (long-term effects) by measuring spirochete bioluminescence in vivo. At the endpoint, bacterial burden was measured in tissues by real-time PCR, and histology was performed to assess differences in the inflammatory response. Between days 10 and 14 post-infection, live imaging showed that mice on a HF diet presented a significantly higher spirochetal burden and greater dissemination than the controls. These differences were transient and restricted to the first two weeks of infection, without long-term effect observed. Histology showed no significant differences in inflammation between HF and control mice. However, qPCR showed that mice fed with HF diet had a higher B. burgdorferi burden in tissues, including heart, visceral, and subcutaneous fat. These findings revealed that high cholesterol levels resulting from a HF diet led to increases in spirochetal burden and dissemination early in the infection, suggesting that cholesterol may contribute to spirochete persistence and associated Lyme disease symptoms.