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Interleukin‐10 protects against blood‐induced joint damage

Summary Despite prophylactic treatment, haemophilia patients suffer from spontaneous joint bleeds, which lead to severe joint damage. Also after joint trauma, an intra‐articular haemorrhage can add to joint damage over time. This study evaluated interleukin 10 (IL‐10) in the search for possible inte...

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Bibliographic Details
Published in:British journal of haematology 2008-09, Vol.142 (6), p.953-961
Main Authors: Jansen, Nathalie W. D., Roosendaal, Goris, Hooiveld, Michel J. J., Bijlsma, Johannes W. J., Van Roon, Joël A. G., Theobald, Matthias, Lafeber, Floris P. J. G.
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Language:English
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Summary:Summary Despite prophylactic treatment, haemophilia patients suffer from spontaneous joint bleeds, which lead to severe joint damage. Also after joint trauma, an intra‐articular haemorrhage can add to joint damage over time. This study evaluated interleukin 10 (IL‐10) in the search for possible interventions to prevent or limit the damaging effects of joint bleeds. Human articular cartilage tissue explants were cultured in the presence or absence of 50% v/v blood (or its cellular components) for 4 d (the expected blood load in vivo after a joint haemorrhage), followed by a recovery period of 12 d. Pharmacological dosages of IL‐10 reached during treatment (1 or 10 ng/ml) were added. Additionally, cartilage and synovial tissue obtained from joints with end‐stage haemophilic arthropathy (HA) were cultured in the presence of IL‐10 (10 ng/ml). IL‐10 protected cartilage from the damaging effects of blood exposure, measured by its effects on proteoglycan turnover. In addition, IL‐10 beneficially influenced cartilage from patients with HA and reduced the production of the inflammatory cytokines IL‐1β and tumour necrosis factor‐α by haemophilic synovial tissue. Taken together, although effects were obtained in vitro, IL‐10 protects against blood‐induced joint damage and might be further evaluated as candidate in treatment of tissue damaging effects of joint haemorrhages.
ISSN:0007-1048
1365-2141
DOI:10.1111/j.1365-2141.2008.07278.x