Treatment and mechanism of fecal microbiota transplantation in mice with experimentally induced ulcerative colitis

Treatment and mechanism of fecal microbiota transplantation in mice with experimentally induced ulcerative colitis
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实验性溃疡性结肠炎小鼠粪便菌群移植的治疗及机制

DOI:
10.1177/15353702211006044
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发表时间:
2021-07-01
影响因子:
3.2
通讯作者:
Liao, Wu
Liao, Wu
中科院分区:
医学4区
文献类型:
--
作者:
Zhang, Leichang;Ma, Xiaofei;Liao, Wu

文献摘要

被引文献

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通过粪便微生物群移植恢复肠道微生物群失调被认为是溃疡性结肠炎的有希望的治疗方法。然而,其缓解作用的机制仍不清楚。溃疡性结肠炎的发病机制与免疫细胞和炎性细胞因子的参与有关。在此,我们旨在研究粪便微生物群移植对葡聚糖硫酸钠诱导的溃疡性结肠炎小鼠模型中T细胞细胞因子的影响。5-氨基水杨酸(5-阿萨)用作阳性对照。将雄性C57 BL/6小鼠随机分为对照组、模型组(UC)、UC + FMT组和UC + 5-阿萨组。每组由5只小鼠组成。通过粪便隐血筛选和苏木精-伊红染色证实小鼠模型的建立。结果显示,粪便微生物群移植减少了结肠炎症,显著降低了辅助性T细胞(Th)1和Th 17细胞,干扰素-γ,白细胞介素-2和白细胞介素-17,以及显著增加了Th 2和调节性T细胞(Treg),白细胞介素-4,白细胞介素-10和转化生长因子-β,并改善了常规血细胞计数。此外,16 S rRNA基因测序分析显示,在溃疡性结肠炎组中,阿克曼氏菌属的相对丰度显著增加,而螺杆菌属的相对丰度显著减少。粪便微生物群移植使肠道微生物群的分布恢复到对照组的分布。这些发现证明了粪便微生物群移植通过调节肠道微生物群改善Th 1/Th 2和Th 17/Treg失衡来控制实验诱导的溃疡性结肠炎的能力。
Restoring intestinal microbiota dysbiosis with fecal microbiota transplantation is considered as a promising treatment for ulcerative colitis. However, the mechanisms underlying its relieving effects remain unclear. Ulcerative colitis pathogenesis is associated with the involvement of immune cells and inflammatory cytokines. Here, we aimed to investigate the effect of fecal microbiota transplantation on T cell cytokines in a dextran sulfate sodium-induced ulcerative colitis mouse model. Five-aminosalicylic acid (5-ASA) was used as the positive control. Male C57BL/6 mice were randomly assigned to control, model (UC), UC + FMT, and UC + 5-ASA groups. Each group consisted of five mice. The establishment of the mouse model was verified by fecal occult-blood screening and hematoxylin–eosin staining. Results showed that fecal microbiota transplantation reduced colonic inflammation, significantly decreased T helper (Th)1 and Th17 cells, interferon-gamma, interleukin-2 and interleukin-17, as well as significantly increased Th2 and regulatory T (Treg) cells, interleukin-4, interleukin-10, and transforming growth factor-beta, and improved routine blood count. Furthermore, 16S rRNA gene-sequencing analysis showed a significant increase in the relative abundance of genus Akkermansia and a significant decrease in the relative abundance of genus Helicobacter in the ulcerative colitis group. Fecal microbiota transplantation restored the profile of the intestinal microbiota to that of the control group. These findings demonstrated the capability of fecal microbiota transplantation in controlling experimentally induced ulcerative colitis by improving Th1/Th2 and Th17/Treg imbalance through the regulation of intestinal microbiota.