Interleukin ‐37 inhibits osteoclastogenesis and alleviates inflammatory bone destruction

Interleukin 37 downregulates osteoclastogenesis through direct and indirect actions AbstractExcessive 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 form ation remains unclear. Next, IL‐37 alleviated the inflammatory bone destruction in the mouse in vivo. We used receptor activator of nuclear factor‐κB ligand and lipopolysaccharide to trigger osteoclastogenesis under physiological and pathological conditions to observe the role of IL‐37 in thi s 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 κBα and p65 and the expression of nuclear factor of a ctivated 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.

Source: Journal of Cellular Physiology - November 10, 2018 Category: Cytology Authors: Ruohui Tang, Jin Yi, Jing Yang, Yueqi Chen, Wei Luo, Shiwu Dong, Jun Fei Tags: ORIGINAL RESEARCH ARTICLE Source Type: research