Mannose ameliorates experimental colitis by protecting intestinal barrier integrity.
Mannose ameliorates experimental colitis by protecting intestinal barrier integrity.
复制标题
甘露糖通过保护肠道屏障完整性改善实验性结肠炎
DOI：
10.1038/s41467-022-32505-8
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发表时间：
2022-08-16
影响因子：
16.6
通讯作者：
中科院分区：
文献类型：
--
作者：
代谢物的改变与炎症性肠病（IBD）的发病机制有关，包括结肠炎。甘露糖是一种天然的生物活性单糖，参与糖蛋白的代谢和合成，具有抗炎和抗氧化活性。我们在这里表明，在IBD患者和实验性结肠炎小鼠中，甘露糖的循环水平升高。甘露糖治疗可减轻两种小鼠结肠炎模型的肠屏障损伤，即葡聚糖硫酸钠（DSS）诱导的结肠炎和il -10缺陷小鼠的自发性结肠炎。我们证明，甘露糖治疗增强溶酶体完整性，限制组织蛋白酶B的释放，防止线粒体功能障碍和肌球蛋白轻链激酶（MLCK）在肠上皮损伤的情况下诱导的紧密连接破坏。甘露糖与美沙拉胺对小鼠结肠炎有协同治疗作用。综上所述，结果表明补充甘露糖可能是治疗结肠炎和其他与肠屏障功能障碍相关疾病的一种可选方法。炎性肠病需要新的潜在疗法，因为并非所有患者对常规疗法都有反应或维持反应。本文作者报道，甘露糖补充剂可能通过对肠上皮溶酶体完整性的影响来改善雄性小鼠的实验性结肠炎。
Metabolite alteration has been associated with the pathogenesis of inflammatory bowel disease (IBD), including colitis. Mannose, a natural bioactive monosaccharide that is involved in metabolism and synthesis of glycoproteins, exhibits anti-inflammatory and anti-oxidative activities. We show here that the circulating level of mannose is increased in patients with IBD and mice with experimental colitis. Mannose treatment attenuates intestinal barrier damage in two mouse colitis models, dextran sodium sulfate (DSS)-induced colitis and spontaneous colitis in IL-10-deficient mice. We demonstrate that mannose treatment enhanced lysosomal integrity and limited the release of cathepsin B, preventing mitochondrial dysfunction and myosin light chain kinase (MLCK)-induced tight junction disruption in the context of intestinal epithelial damage. Mannose exerts a synergistic therapeutic effect with mesalamine on mouse colitis. Cumulatively, the results indicate that mannose supplementation may be an optional approach to the treatment of colitis and other diseases associated with intestinal barrier dysfunction. New potential therapies for inflammatory bowel disease are needed as not all patients respond to or maintain a response to conventional therapies. Here the authors report that mannose supplementation ameliorates experimental colitis in male mice, potentially via effects on intestinal epithelium lysosomal integrity.
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