Vancomycin-resistant Enterococcus (VRE) caused nosocomial infections are rising globally. Multiple measures have been investigated to address this issue, altering gut microbiota through dietary intervention represents one of such effort. Stachyose can promote probiotic growth, which makes it a good candidate for potentially inhibiting VRE infection. This study aimed to determine whether stachyose inhibits VRE colonization and investigated the involvement of gut microbiota this effect of stachyose. In VRE-infection experiment, 6-week old female C57/6 J mice pre-treated with vancomycin were infected with 2 × 10⁸ CFU VRE via gavage. These mice then received oral administration of stachyose or PBS as control for 7days. Two groups of uninfected mice were also received daily gavage of stachyose or PBS for 7 days to observe the impact of stachyose treatment on normal mice. Fresh fecal and colon samples were collected, then VRE colonization, gut microbiota and gene expression were respectively assessed using cultivation, 16s rRNA sequencing and RNA-sequencing in two parallel experiment, respectively. In VRE-infected mice, stachyose treatment significantly reduced VRE colonization on days 9 and 10 post-infection. Stachyose treatment increased the relative abundance of Porphyromonadaceae, Parabacteroides, and Parabacteroides distasonis compared to the PBS-treated infection mice (P < 0.01). Uninfected mice treated with stachyose showed a significant increase in Lactobacillaceae and Lactobacillus compared to the PBS-treated uninfected mice(P < 0.05). RNA-sequencing results showed that stachyose treatment in VRE-infected mice increased expression of genes involved in TNF and IL-17 signaling pathways. Stachyose treatment also up-regulated Hsd17b14, Cyp3a44, Arg1, and down-regulated Pnliprp2, Ces1c, Pla2g4c genes involving in metabolic pathway in uninfected mice. In conclusion, stachyose supplementation can effectively inhibit VRE colonization and probably altering composition of the microbiome, which can in turn result in changes in expression of genes. Stachyose may also benefit health by increasing the abundance of Lactobacillus and expression of genes involving in metabolic pathway in normal mice.

耐万古霉素肠球菌(VRE) 引起的院内感染在全球范围内呈上升趋势。已经研究了多种措施来解决这个问题，通过饮食干预改变肠道微生物群是其中一项努力。水苏糖可以促进益生菌生长，这使其成为潜在抑制 VRE 感染的良好候选者。本研究旨在确定水苏糖是否抑制 VRE 定植，并调查了肠道微生物群对水苏糖的这种影响的参与。在VRE感染实验中，用万古霉素预处理的6周龄雌性C57/6 J小鼠感染2×10 ⁸ CFU VRE 通过管饲法。然后这些小鼠口服水苏糖或 PBS 作为对照，持续 7 天。两组未感染小鼠也每天灌胃水苏糖或PBS 7天，观察水苏糖处理对正常小鼠的影响。收集新鲜粪便和结肠样本，然后分别使用培养、16s rRNA 测序和 RNA 测序在两个平行实验中分别评估 VRE 定植、肠道微生物群和基因表达。在 VRE 感染的小鼠中，水苏糖处理显着减少了感染后第 9 天和第 10 天的 VRE 定植。水苏糖处理增加了卟啉单胞菌科、Parabacteroides和Parabacteroides distasonis的相对丰度与 PBS 处理的感染小鼠相比 (P < 0.01)。与PBS处理的未感染小鼠相比，水苏糖处理的未感染小鼠的乳杆菌科和乳酸杆菌显着增加（P < 0.05）。RNA 测序结果表明，在 VRE 感染的小鼠中，水苏糖处理增加了参与 TNF 和 IL-17 信号通路的基因的表达。水苏糖处理还上调Hsd17b14、Cy​​p3a44、Arg1和下调Pnliprp2、Ces1c、Pla2g4c参与未感染小鼠代谢途径的基因。总之，水苏糖补充剂可以有效抑制 VRE 定植，并可能改变微生物组的组成，进而导致基因表达的变化。水苏糖还可以通过增加正常小鼠中乳酸杆菌的丰度和参与代谢途径的基因的表达来有益于健康。