Lyme disease is caused by the bacterium Borrelia burgdorferi, transmitted through tick bites. While most cases resolve with antibiotics, a significant subset of patients experience Post-Treatment Lyme Disease Syndrome (PTLDS) — persistent symptoms including fatigue, cognitive dysfunction, joint pain, and neurological symptoms that continue long after the infection is cleared. The dominant hypothesis for PTLDS is that the infection triggers an immune dysregulation that perpetuates even without active bacteria.
The MSC Rationale in Lyme/PTLDS
MSC therapy targets the immune dysregulation of PTLDS rather than the Borrelia infection itself. Key mechanisms include:
Immune Rebalancing
MSCs release immunomodulatory factors including TGF-β, IL-10, and PGE2, which rebalance the immune system following dysregulation triggered by Borrelia exposure. They reduce excessive T-cell activation, suppress pro-inflammatory Th17 cells, and boost regulatory T-cells (Tregs) — reducing the immune-mediated tissue damage that drives PTLDS symptoms.
Anti-Inflammatory Action on Joint and Nerve Tissue
Joint pain, neuropathy, and fatigue in PTLDS are largely inflammation-driven rather than infection-driven. MSCs suppress the local joint inflammation (similar to RA), reduce neuroinflammation contributing to brain fog and neuropathy, and provide systemic anti-inflammatory benefit that may address the fatigue component.
Important Distinction
MSC therapy for Lyme is appropriate for patients with confirmed PTLDS — documented prior Lyme infection, completed antibiotic treatment, and persistent symptoms without evidence of active infection. It is not a treatment for active Borrelia infection, which requires standard antibiotic management. This distinction is evaluated on your medical records review before any protocol is offered.