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Elevated interleukin (IL)-1 concentrations in synovial fluid have been implicated in joint bone and cartilage destruction. Previously, we showed that IL-1 β  stimulated the expression of prostaglandin (PG) receptor EP4 via increased PGE 2  production. However, the effect of IL-1 β  on osteoclast formation via chondrocytes is unclear. Therefore, we examined the effect of IL-1 β  and/or celecoxib on the expression of macrophage colony-stimulating factor (M-CSF), receptor activator of NF- κ B ligand (RANKL), and osteoprotegerin (OPG) in human chondrocytes, and the indirect effect of IL-1 β  on osteoclast-like cell formation using RAW264.7 cells. OPG and RANKL expression increased with IL-1 β ; whereas M-CSF expression decreased. Celecoxib blocked the stimulatory effect of IL-1 β . Conditioned medium from IL-1 β -treated chondrocytes decreased TRAP staining in RAW264.7 cells. These results suggest that IL-1 β  suppresses the formation of osteoclast-like cells via increased OPG production and decreased M-CSF production in chondrocytes, and OPG production may increase through an autocrine mechanism involving celecoxib-related PGs.

mediators of inflammation

IL-1β Suppresses the Formation of Osteoclasts by Increasing OPG Production via an Autocrine Mechanism Involving Celecoxib-Related Prostaglandins in Chondrocytes