Lentinan Exerts its Anti-Inflammatory Activity by Suppressing TNFR1 Transfer to the Surface of Intestinal Epithelial Cells through Dectin-1 in an in vitro and mice model

Kana Sakaguchi, Y. Shirai, T. Itoh, M. Mizuno
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引用次数: 3

Abstract

It has been reported that lentinan, β-1,3; 1,6-glucan derived from Lentinula edodes, suppresses intestinal inflammation and ameliorates symptoms of colitis. However, the mechanism of intestinal anti-inflammatory activity of lentinan and how it is recognized by intestinal epithelial cells remains largely unclear. The receptor for lentinan on intestinal epithelial cells was identified using an in vitro gut inflammation model consisting of Caco-2 and RAW264.7 cells. Colitis was induced in 7 to 8 week-old wild-type (WT) or knockout (KO) mice by the free intake of water containing 2% dextran sulfate sodium (DSS) for 7 days. Lentinan was administered daily via intragastric administration. Tumor necrosis factor receptor 1 (TNFR1)-GFP complex was constructed to monitor its movement in Caco-2 cells using confocal and total internal fluorescence microscopy. The results indicated that lentinan suppressed DSS-induced body weight loss, shortening of colon length, histological score, and inflammatory cytokine mRNA expression in the inflamed tissues of WT mice, whereas these suppressive effects of lentinan were not observed in Dectin-1 KO mice. Furthermore, lentinan reduced TNFR1 expression in intestinal epithelial cells of WT mice but not those from Dectin-1 KO mice. Using TNFR1-GFP constructs, it was confirmed that lentinan reduced TNFR1 expression on Caco-2 cell membranes through Dectin-1 ligation. Our study revealed that lentinan suppressed intestinal inflammation by Dectin-1-mediated regulation of TNFR1 transfer to the surface of intestinal epithelial cells.
在体外和小鼠模型中,香菇多糖通过Dectin-1抑制TNFR1向肠上皮细胞表面的转移,从而发挥其抗炎活性
据报道,香菇多糖β-1,3;从香菇中提取的1,6-葡聚糖可抑制肠道炎症并改善结肠炎症状。然而,香菇多糖的肠道抗炎作用机制及其如何被肠上皮细胞识别仍不清楚。采用Caco-2和RAW264.7细胞组成的体外肠道炎症模型,鉴定香菇多糖对肠上皮细胞的受体。以7 ~ 8周龄野生型(WT)或基因敲除型(KO)小鼠为研究对象,连续7天自由饮水2%葡聚糖硫酸钠(DSS)诱导结肠炎。香菇多糖每天灌胃给药。构建肿瘤坏死因子受体1 (TNFR1)-GFP复合物,利用共聚焦和全内荧光显微镜监测其在Caco-2细胞中的运动。结果表明,香菇多糖可抑制dss诱导的WT小鼠体重减轻、结肠长度缩短、组织学评分和炎症细胞因子mRNA表达,而在Dectin-1 KO小鼠中未观察到香菇多糖的这些抑制作用。此外,香菇多糖降低了WT小鼠肠上皮细胞中TNFR1的表达,而Dectin-1 KO小鼠则没有。利用TNFR1- gfp构建体,证实香菇多糖通过Dectin-1连接降低了Caco-2细胞膜上TNFR1的表达。我们的研究表明,香菇多糖通过dectin -1介导的TNFR1向肠上皮细胞表面转移来抑制肠道炎症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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