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

利用Dectin-1的胞外区作为β-葡聚糖的特异性探针，我们成功地检测到巨噬细胞株和小鼠腹膜巨噬细胞分泌的可溶性和Dectin-1反应性的b-葡聚糖，这些巨噬细胞吞噬了不溶的b-葡聚糖颗粒。含有释放的β-葡聚糖的RAW264.7细胞培养上清刺激RAW264.7细胞，导致细胞因子的诱导表达。巨噬细胞释放Dectin-1反应性b-葡聚糖可被NADPH氧化酶抑制剂或自由基清除剂抑制。这些结果表明，降解的但Dectin-1活性的b-葡聚糖是从巨噬细胞释放出来的，吞噬不溶性的b-葡聚糖颗粒，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.