title: Interleukin-10 protects against blood-induced joint damage.
abstract: 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-1beta and tumour necrosis factor-alpha 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.
authors.affiliation: Rheumatology & Clinical Immunology, UMC Utrecht, The Netherlands. n.w.d.jansen@umcutrecht.nl
authors.forename: Nathalie W D
authors.initials: NW
authors.lastname: Jansen
authors.forename: Goris
authors.initials: G
authors.lastname: Roosendaal
authors.forename: Michel J J
authors.initials: MJ
authors.lastname: Hooiveld
authors.forename: Johannes W J
authors.initials: JW
authors.lastname: Bijlsma
authors.forename: Joël A G
authors.initials: JA
authors.lastname: van Roon
authors.forename: Matthias
authors.initials: M
authors.lastname: Theobald
authors.forename: Floris P J G
authors.initials: FP
authors.lastname: Lafeber
mesh_terms: D001769:Blood; D002358:Cartilage, Articular / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D004353:Drug Evaluation, Preclinical / Q000379:methods; D004912:Erythrocytes / Q000502:physiology; D006395:Hemarthrosis / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D006467:Hemophilia A / Q000150:complications; D006801:Humans; D016753:Interleukin-10 / Q000494:pharmacology*; D053583:Interleukin-1beta / Q000096:biosynthesis; D007963:Leukocytes, Mononuclear / Q000502:physiology; D008297:Male; D011509:Proteoglycans / Q000378:metabolism; D013583:Synovial Membrane / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D046509:Tissue Culture Techniques; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D053583:Interleukin-1beta; D011509:Proteoglycans; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10