Glycerol monolaurate ameliorates DSS-induced acute colitis by inhibiting infiltration of Th17, neutrophils, macrophages and altering the gut microbiota.
Glycerol monolaurate ameliorates DSS-induced acute colitis by inhibiting infiltration of Th17, neutrophils, macrophages and altering the gut microbiota.
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DOI：
10.3389/fnut.2022.911315
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发表时间：
2022
影响因子：
5
通讯作者：
Guleng, Bayasi
中科院分区：
文献类型：
--
作者：
He, Ke-Jie;Dong, Jia-Hui;Ouyang, Xiao-Mei;Huo, Ya-Ni;Cheng, Xiao-Shen;Lin, Ying;Li, Yue;Gong, Guoyu;Liu, Jingjing;Ren, Jian-Lin;Guleng, Bayasi
炎症性肠病（IBD）由于反复和长期发作，给国家和家庭带来了沉重的医疗负担，并且在世界范围内IBD的发病率和患病率正在增加。因此，找到一种有效的治疗方法是一件非常紧迫的事情。单月桂酸甘油（GML）有12个碳链，是一种天然存在于人类母乳中的化合物。一些研究表明，GML具有抗菌和抗炎作用。然而，具体的作用机制尚不清楚。使用3% DSS建立小鼠急性结肠炎，并给予单月桂酸甘油（500 mg·kg - 1）两周。采用QPCR和western blotting检测炎症状态。所描述的小鼠接受流式细胞术分析免疫细胞活化。GML治疗后，dss性结肠炎小鼠结肠缩短、脾脏重量增加等宏观症状得到缓解，体重减轻。此外，GML降低促炎因子（NF-α、IL-1β、IL-1α）表达，升高抗炎因子（IL-10、TGF-β）表达。GML抑制MAPK和NF-κB信号通路的激活，改善组织损伤，增加肠紧密连接蛋白的表达。此外，通过流式细胞术提取的肠组织lpmc显示，GML处理导致Th17细胞、中性粒细胞和巨噬细胞减少，16S rDNA测序显示GML增加了Akkermansia和Lactobacillus murinus等共生菌的丰度。我们发现口服GML通过抑制Th17细胞、中性粒细胞和巨噬细胞的浸润、保护肠粘膜屏障和改变共生菌的丰度来改善dss诱导的结肠炎。这项研究为GML治疗IBD的生物学功能和治疗潜力提供了新的见解。
Inflammatory bowel disease (IBD) places a heavy medical burden on countries and families due to repeated and prolonged attacks, and the incidence and prevalence of IBD are increasing worldwide. Therefore, finding an effective treatment is a matter of great urgency. Glycerol monolaurate (GML), which has a twelve-carbon chain, is a compound naturally found in human breast milk. Some studies have shown that GML has antibacterial and anti-inflammatory effects. However, the specific mechanism of action remains unclear. Acute colitis was established in mice using 3% DSS, and glycerol monolaurate (500 mg·kg−1) was administered for two weeks. QPCR and western blotting were performed to examine the inflammatory status. Mice described were subjected to flow cytometry analysis for immune cell activation. GML treated alleviated macroscopic symptoms such as shortened colons, increased spleen weight, and caused weight loss in mice with DSS-induced colitis. In addition, GML decreased the expression of pro-inflammatory factors (NF-α, IL-1β and IL-1α) and increased the expression of anti-inflammatory factors (IL-10 and TGF-β). GML inhibited the activation of the MAPK and NF-κB signalling pathways, improved tissue damage, and increased the expression of intestinal tight junction proteins. In addition, LPMCs extracted from intestinal tissue via flow cytometry showed that GML treatment led to a decrease of Th17 cells, Neutrophils and Macrophages. 16S rDNA sequencing showed that GML increased the abundance of commensal bacterium such as Akkermansia and Lactobacillus murinus. We showed that oral administration of GML ameliorated DSS-induced colitis by inhibiting infiltration of Th17 cells, Neutrophils, and Macrophages, protecting the intestinal mucosal barrier and altered the abundance of commensal bacterium. This study provides new insights into the biological function and therapeutic potential of GML in the treatment of IBD.
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影响因子：
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