ArticleRMD open2025
Evaluating the role of lipopolysaccharides in the joint: fibronectin as a novel protective mechanism.
Article in RMD open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- Venom-Derived Proteins fromInternational journal of molecular sciences · 2026Article
- Gut and Joint Microbiome and Dysbiosis: A New Perspective on the Pathogenesis and Treatment of Osteoarthritis.Pathogens (Basel, Switzerland) · 2026Review
- "Gut-Joint Axis" Perspective on Immunometabolic Crosstalk in Osteoarthritis: A Narrative Review of Mechanistic Insights and Targeted Strategies.Journal of inflammation research · 2026Review
Corrections and comments
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Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the presence and bioactivity of lipopolysaccharides (LPS) in synovial fluid (SF) of osteoarthritis (OA) patients and elucidate mechanisms modulating their inflammatory potential.
methodsSF samples from 56 OA, 7 rheumatoid arthritis and 39 trauma patients were analysed for LPS concentration and bioactivity. Lipid A composition was assessed using liquid chromatography-mass spectrometry (LC-MS). In a rat model, LPS was administered systemically for 32 days to evaluate its impact on joint degeneration. The interaction between LPS and synovial proteins, particularly fibronectin (Fn), was examined through in vitro assays and a 3D synovial membrane model.
resultsLPS was detected in all SF samples with comparable concentrations and lipid A profiles across all groups. LC-MS measurements indicated higher LPS levels than those obtained from standard endotoxin assays, suggesting limitations in conventional detection methods. Despite elevated LPS presence, bioactivity assays revealed minimal proinflammatory responses, implying the existence of intrinsic SF factors neutralising LPS. In vivo, prolonged systemic LPS exposure did not induce OA-like changes in rat joints. Notably, LPS colocalised with Fn in the synovial membrane, and Fn binding attenuated LPS bioactivity and hindered its migration in vitro.
conclusionsLPS is prevalent in SF across various joint conditions but exhibits low bioactivity, indicating it is not a primary driver of joint inflammation. Fn plays a crucial role in sequestering and neutralising LPS within the synovial environment, offering a protective mechanism against LPS-induced inflammation. These findings underscore the need for accurate LPS measurement techniques and suggest potential therapeutic targets for modulating joint inflammation.
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