Degradation of b-glucan absorbed from intestine and the effect of degraded b-glucan on the intestinal immune function

使用Dectin-1的细胞外结构域作为b-葡聚糖特异性探针，我们成功地检测了从巨噬细胞系以及小鼠腹腔巨噬细胞中排出的可溶性和Dectin-1反应性b-葡聚糖，这些巨噬细胞吞噬了不溶性b-葡聚糖颗粒。含有排出的β-葡聚糖的RAW 264.7细胞培养物上清液刺激RAW 264.7细胞，导致细胞因子表达的诱导。这种Dectin-1反应性β-葡聚糖从巨噬细胞中的释放受到NADPH氧化酶抑制剂或自由基清除剂的抑制。 这些结果表明，降解但Dectin-1反应性的b-葡聚糖从吞噬不溶性b-葡聚糖颗粒的巨噬细胞中排出，并刺激其他吞噬细胞。

Using the extracellular domain of Dectin-1 as b-glucan-specific probes, we succeeded in detection of soluble and Dectin-1-reactive b-glucan discharged from macrophage cell lines as well as mouse peritoneal macrophages, which had phagocytized insoluble b-glucan particles. The RAW264.7 cell culture-supernatant containing the discharged b-glucan stimulated RAW264.7 cells, resulting in the induction of cytokine expression. Such discharge of Dectin-1-reactive b-glucan from macrophage cells was inhibited by either NADPH oxidase inhibitors or radical scavengers. These results suggest that degraded but Dectin-1-reactive b-glucan is discharged from macrophage cells phagocytizing insoluble b-glucan particles and stimulates the other phagocytes.