OBJECTIVE: To examine the effect of human interleukin-17 (IL-17) on nitric oxide (NO) production in human osteoarthritis (OA) cartilage under ex vivo conditions. METHODS: OA cartilage from patients undergoing knee replacement surgery was used in explant assays to assess the effect of IL-17. NO production was measured by estimating the stable NO metabolite, nitrite, in conditioned medium. RESULTS: IL-17 augmented the spontaneous production of nitric oxide. This augmentation was sensitive to cycloheximide and pyrrolidine dithiocarbamate, but not to dexamethasone or soluble IL-1 receptor. CONCLUSION: IL-17 augments nitric oxide production in OA cartilage via nuclear factor kappaB activation, but independently of IL-1beta signaling.
OBJECTIVE: To examine the effect of humaninterleukin-17 (IL-17) on nitric oxide (NO) production in humanosteoarthritis (OA) cartilage under ex vivo conditions. METHODS: OA cartilage from patients undergoing knee replacement surgery was used in explant assays to assess the effect of IL-17. NO production was measured by estimating the stable NO metabolite, nitrite, in conditioned medium. RESULTS:IL-17 augmented the spontaneous production of nitric oxide. This augmentation was sensitive to cycloheximide and pyrrolidine dithiocarbamate, but not to dexamethasone or soluble IL-1 receptor. CONCLUSION:IL-17 augments nitric oxide production in OA cartilage via nuclear factor kappaB activation, but independently of IL-1beta signaling.