Development of biopolymer compound to elucidate the effect of glucan on innate immune system

据报道，一些免疫系统细胞表面受体与破骨细胞的形成有关。Dectin-1是一种β-葡聚糖的凝集素受体，主要存在于髓系细胞上。在本研究中，我们研究了Dectin-1激动剂Curdlan对破骨细胞生成的影响。在DECIN-1高表达的RAW 264.7细胞(d-RAW)中，Curdlan抑制核因子-kappaB受体激活剂配体(RANKL)诱导的破骨细胞分化、骨吸收和肌动蛋白环的形成。此外，Curdlan还抑制RANKL诱导的活化T细胞胞浆核因子1(NFATc1)的表达。这表明Curdlan-Dectin-1相互作用的激活对破骨细胞形成所需的基因起着关键的调节作用。

Several immune system cell-surface receptors are reported to be associated with osteoclastogenesis. Dectin-1, a lectin receptor for beta-glucan, is found predominantly on cells of the myeloid lineage. In the present study, we examined the effect of dectin-1 agonist, curdlan, on osteoclastogenesis. In dectin-1 over-expressing RAW 264.7 cells (d-RAW), curdlan suppressed receptor activator of nuclear factor-kappaB (NF-kappaB) ligand (RANKL)-induced osteoclast differentiation, bone resorption and actin-ring formation. Furthermore, curdlan inhibited RANKL-induced nuclear factor of activated T-cell cytoplasmic 1 (NFATc1) expression.In conclusion, our results demonstrate that curdlan potentially inhibits osteoclast differentiation, especially NFATc1 expression. This suggests activation of curdlan-dectin-1 interaction critically regulates the genes required for osteoclastogenesis.