Even after antibiotic treatment, some Lyme disease patients continue to suffer from debilitating arthritis. A new Yale study may explain why.
The tick-borne bacterium Borrelia burgdorferi leaves behind parts of its cell wall in patients’ joints, which appears to trigger an immune reaction that contributes to the inflammation observed in Lyme arthritis patients, the researchers report in the journal Proceedings of the National Academy of Sciences.
This study — led by the lab of Christine Jacobs-Wagner, the William H. Fleming, M.D. Professor of Molecular, Cellular, and Developmental Biology and professor of microbial pathogenesis — found peptidoglycan, a major component of bacterial cell walls, in the joint fluid of patients who had received intensive antibiotic treatment for Lyme arthritis. Also, in a mouse model, the Borrelia peptidoglycan was found to cause joint inflammation.
“Our research shows that the Borrelia peptidoglycan is likely playing an important role in triggering and perpetuating arthritis in some patients,” Jacobs-Wagner said. “Hopefully, our findings will inform the development of better treatments for these patients.”
The work was done in collaboration with the labs of Linda Bockenstedt at the Yale School of Medicine, Allen Steere at Massachusetts General Hospital, and Waldemar Vollmer at Newcastle University.