Borrelia burgdorferi peptidoglycan is a persistent antigen in patients with Lyme arthritis
Three articles on PainSci cite Jutras 2019: 1. The Complete Guide to Trigger Points & Myofascial Pain 2. 35 Surprising Causes of Pain 3. A Rational Guide to Fibromyalgia
PainSci commentary on Jutras 2019: ?This page is one of thousands in the PainScience.com bibliography. It is not a general article: it is focused on a single scientific paper, and it may provide only just enough context for the summary to make sense. Links to other papers and more general information are provided wherever possible.
The Borrelia burgdorferi bacteria causes Lyme disease, but many people continue to suffer even when all the B. burgodorferi are dead — a previously unexplained phenomenon called chronic Lyme disease, about which there are many pseudoscientific ideas and treatments. But there’s never been much doubt that some people seem to suffer long after an acute Lyme infection.
This research identifies a likely cause for that suffering: a lingering molecule produced by the bacteria during their campaign. They discovered that B. burgodorferi sheds a peptidoglycan (PGBb) molecule while it grows, which collects in joints especially and continues to provoke an immune system response, causing ongoing inflammation and malaise.
Although “just one study” of a controversial topic, it was quite a persuasive one, especially the part where they induced acute arthritis in mice by injecting them with PGBb.
If correct, then this study has solved one of the bigger puzzles in medicine — a big deal.
original abstract †Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.
Lyme disease is a multisystem disorder caused by the spirochete Borrelia burgdorferi A common late-stage complication of this disease is oligoarticular arthritis, often involving the knee. In ∼10% of cases, arthritis persists after appropriate antibiotic treatment, leading to a proliferative synovitis typical of chronic inflammatory arthritides. Here, we provide evidence that peptidoglycan (PG), a major component of the B. burgdorferi cell envelope, may contribute to the development and persistence of Lyme arthritis (LA). We show that B. burgdorferi has a chemically atypical PG (PGBb) that is not recycled during cell-wall turnover. Instead, this pathogen sheds PGBb fragments into its environment during growth. Patients with LA mount a specific immunoglobulin G response against PGBb, which is significantly higher in the synovial fluid than in the serum of the same patient. We also detect PGBb in 94% of synovial fluid samples (32 of 34) from patients with LA, many of whom had undergone oral and intravenous antibiotic treatment. These same synovial fluid samples contain proinflammatory cytokines, similar to those produced by human peripheral blood mononuclear cells stimulated with PGBb In addition, systemic administration of PGBb in BALB/c mice elicits acute arthritis. Altogether, our study identifies PGBb as a likely contributor to inflammatory responses in LA. Persistence of this antigen in the joint may contribute to synovitis after antibiotics eradicate the pathogen. Furthermore, our finding that B. burgdorferi sheds immunogenic PGBb fragments during growth suggests a potential role for PGBb in the immunopathogenesis of other Lyme disease manifestations.
This page is part of the PainScience BIBLIOGRAPHY, which contains plain language summaries of thousands of scientific papers & others sources. It’s like a highly specialized blog. A few highlights:
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