Dectin‐1–mediated suppression of RANKL‐induced osteoclastogenesis by glucan from baker's yeast

Immunoreceptors expressed on osteoclast precursor cells modify osteoclast differentiation and bone resorption activity. Dectin‐1 is a lectin receptor of β‐glucan and is specifically expressed in osteoclast precursor cells. In this study, we evaluated the bioactivity of β‐glucan on receptor activator of nuclear factor‐kappa B ligand (RANKL)‐induced osteoclastogenesis and observed that glucan from baker's yeast inhibited this process in mouse bone marrow cells and dectin‐1–overexpressing RAW264.7 (d‐RAW) cells. In conjunction, RANKL‐induced nuclear factor of activated T cell c1 expression was suppressed, subsequently downregulating TRAP and Oc‐stamp. Additionally, nuclear factor‐kappa B activation and the expression of c‐fos and Blimp1 were reduced in d‐RAW cells. Furthermore, glucan from baker's yeast induced the degradation of Syk protein, essential factor for osteoclastogenesis. These results suggest that glucan from baker's yeast suppresses RANKL‐induced osteoclastogenesis and can be applied as a new treatment strategy for bone‐related diseases. Graphical β‐glucan inhibits osteoclast formation. β‐glucan attenuates nuclear factor‐kappa B activation and Blimp1 expression. β‐glucan degrades syk protein.