Abstract：
This study aimed to investigate the hypothesis that dietary konjac glucomannan (KGM) could alleviate Salmonella typhimurium-induced colitis by modulating intestinal microbiota. Mice were fed an isocaloric and isofibrous diet supplemented with either 7% KGM or cellulose and were treated with 5 × 108 CFU of S. typhimurium. The results showed that KGM had an average molecular weight of 936 kDa and predominantly consisted of mannose and glucose at a molar ratio of 1:1.22. In vivo studies demonstrated that dietary KGM effectively mitigated colonic lesions, oxidative stress, disruption of tight junction protein 2 and occludin, and the inflammatory response induced by S. typhimurium. Moreover, KGM administration alleviated the dramatic upregulation of toll-like receptor 2 (TLR2) and phosphonuclear factor κB (NF-κB) protein abundance, induced by Salmonella treatment. Notably, dietary KGM restored the reduced Muribaculaceae and Lactobacillus abundance and increased the abundance of Blautia and Salmonella in S. typhimurium-infected mice. Spearman correlation analysis revealed that the gut microbiota improved by KGM contribute to inhibit inflammation and oxidative stress. These results demonstrated the protective effects of dietary KGM against colitis by modulating the gut microbiota and the TLR2-NF-κB signaling pathway in response to Salmonella infection.
摘要：
本研究旨在探讨饮食魔芋葡甘露聚糖(KGM)通过调节肠道菌群减轻鼠伤寒沙门氏菌诱导的结肠炎的假说。给小鼠喂食补充有7%KGM或纤维素的等热量和等纤维饮食,并用5×108CFU的鼠伤寒沙门氏菌处理。结果显示KGM具有936kDa的平均分子量,并且主要由甘露糖和葡萄糖以1:1.22的摩尔比组成。体内研究表明，饮食KGM有效缓解结肠病变，氧化应激，紧密连接蛋白2和闭合蛋白的破坏，和鼠伤寒沙门氏菌诱导的炎症反应。此外，KGM给药减轻了toll样受体2（TLR2）和磷核因子κB（NF-κB）蛋白丰度的急剧上调，由沙门氏菌治疗诱导。值得注意的是,饮食KGM恢复了鼠伤寒沙门氏菌感染小鼠中减少的Muribaculaceae和乳酸杆菌的丰度，并增加了布劳特氏菌和沙门氏菌的丰度。Spearman相关分析显示，KGM改善的肠道菌群有助于抑制炎症和氧化应激。这些结果证明了饮食KGM通过调节肠道菌群和TLR2-NF-κB信号通路响应沙门氏菌感染而对结肠炎的保护作用。
