Excessive osteoclast formation is one of the important pathological features of inflammatory bone destruction.Interleukin-37(IL-37)is an anti-inflammatory agent that is present throughout the body,but it displays low physiological retention.In our study,high levels of the IL-37 protein were detected in clinical specimens from patients with bone infections.However,the impact of IL-37 on osteoclast formation remains unclear.Next,IL-37 alleviated the inflammatory bone destruction in the mouse in vivo.We used receptor activator of nuclear factor-?B ligand and lipopolysaccharide to trigger osteoclastogenesis under physiological and pathological conditions to observe the role of IL-37 in this process and explore the potential mechanism of this phenomenon.In both induction models,IL-37 exerted inhibitory effects on osteoclast differentiation and bone resorption.Furthermore,IL-37 decreased the phosphorylation of inhibitor of ?B? and p65 and the expression of nuclear factor of activated T cells c1,while the dimerization inhibitor of myeloid differentiation factor 88 reversed the effects.These data provide evidence that IL-37 modulates osteoclastogenesis and a theoretical basis for the clinical application of IL-37 as a treatment for bone loss–related diseases. |