Objective: Osteoclast development mediated by osteoblast at inflammation site results in bone resorption. IL-23 is a heterodimeric cytokine and has recently been demonstrated playing a critical role in inflammatory diseases. The aim of this study was to assess the role of IL-23 in osteoblast and osteoclast.
Methods: Bone marrow stromal cell from DBA-1 mice and MC3T3 cell were stimulated by LPS, the subunits of IL-23 was tested by means of RT-PCR and ELISA. Bone marrow macrophages from mice and RAW264.7 cell were as osteoclast precursor to culture osteoclast with IL-23. TRAP staining was performed at day 7 and TRAP positive cell with more than three nuclear were counted as an osteoclast. FACS staining was used for RANK expression on RAW264.7 cell. RT-PCR for analysis of gene transcription of cathepsin K and RANK.
Results: The subunits of IL-23, p19 and p40 were detected when osteoblast stimulated by LPS. The number of osteoclast were increased when IL-23 was added in culture medium. The increased osteoclast formation was associated with enhanced cathepsin K expression which indicated the function of osteoclast for bone resorption. Further more, we found IL-23 up-regulated RANK expression in osteoclast precursor cells. The precursor cell treated with IL-23 developed more osteoclast cells with sequentially culture in present of RANKL.
Conclusions: Osteoblast could express IL-23 when stimulated by LPS. IL-23 promoted osteoclast formation by acting on osteoclast precursor cell directly for up-regulation of RANK expression. This result from provided a role of IL-23 on osteoblast and osteoclast in inflammatory bone resorption.