Bacterial and host enzymes modulate the inflammatory response produced by the peptidoglycan of the Lyme disease agent.

ABSTRACT: The spirochete Borrelia burgdorferi causes Lyme disease. In some patients, an excessive, dysregulated proinflammatory immune response can develop in joints leading to persistent arthritis even after antibiotic therapy. In such patients, persistence of antigenic B. burgdorferi peptidoglycan (PG^Bb) fragments within joint tissues may contribute to immunopathogenesis pre- and post-antibiotic treatment. In live B. burgdorferi cells, the outer membrane shields the polymeric PG^Bb sacculus from exposure to the immune system. However, unlike most diderm bacteria, B. burgdorferi releases PG^Bb turnover products into its environment due to the absence of recycling activity. In this study, we identified the released PG^Bb fragments

SUBMITTER: McCausland JW 

PROVIDER: S-EPMC11741416 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature