Lyme disease is caused by Borrelia burgdorferi infection, which is transmitted via a tick vector. Lyme arthritis can be a postinfection, inflammatory complication of Lyme disease. Treatment with immunosuppressive agents is effective, which indicates that this disease is mediated by the immune system. Previous work has shown that B. burgdorferi produces peptidoglycan during growth, fragments of which can be detected in the synovial tissue of individuals with Lyme arthritis. How the B. burgdorferi peptidoglycan persists and drives chronic, postinfectious Lyme disease complications remains unclear. Two complimentary studies have now been published that provide insights into B. burgdorferi persistence and identify a potential treatment for Lyme disease.

McClune et al. used a mouse model that enabled real-time tracking of B. burgdorferi peptidoglycan and found that, unlike other peptidoglycans, it accumulates in the liver and persists for weeks, altering the immune profile of the liver. Analysis of synovial samples from individuals with Lyme arthritis showed that polymeric B. burgdorferi peptidoglycan, rather than fragments, persists in the synovium. Together, these findings indicate that B. burgdorferi-derived peptidoglycan might act as a persistent source of antigen that drives chronic inflammation in Lyme arthritis and other complications of Lyme disease.