Gu Wenchao, Zhang Liangkun, Han Tao, Huang Hailiang, Chen Jian
Department of Traditional Chinese Medicine, Central Hospital Affiliated to ShanDong First Medical University (Jinan Central Hospital), Jinan, 250000, People's Republic of China.
Shandong University of Traditional Chinese Medicine, Jinan, 250355, People's Republic of China.
J Inflamm Res. 2022 Apr 24;15:2631-2647. doi: 10.2147/JIR.S358807. eCollection 2022.
An animal model of DSS-induced UC has been widely used in basic research, and the dysbiosis of gut microbiome is one of the important pathogenetic mechanisms of DSS-induced UC, but its dynamic changes and correlation with inflammatory factors are not clear yet.
Clinical signs and tissue damage degree of C57BL/6 ulcerative colitis mice model induced by different concentrations of DSS were compared with that of normal mice, and finally the optimal concentration of DSS was determined. Then we analyzed the sequencing results of gut microbiome and inflammatory factors to determine the dynamic patterns of gut microbiome and their correlation with the inflammatory factors.
DSS at 2.5% and 3.0% concentration could cause intestinal injury and induce colitis. However, 3.0% DSS resulted in higher mortality. In addition, there were dynamic changes of gut microbiome in DSS-induced UC model: the relative abundance of intestinal flora increased first and then decreased in , , , Clostridium_sensu_stricto_1, Lachnospiraceae_NK4A136_group, norank_f_norank_o_Clostridia_UCG-014, , and decreased first and then increased in , , norank_f_Muribaculaceae, in addition, , Coriobacteriaceae_UCG-002 and did not change in the first 14 days but increased significantly on day 21. Moreover, inflammatory cytokines were closely associated with the imbalance of the intestinal microbiota in mice with UC: most pathogenic bacteria in the intestinal tract of the UC animal model were positively correlated with pro-inflammatory factors and negatively correlated with anti-inflammatory factors, while beneficial bacteria were the opposite.
Intestinal microecology plays an important role in DSS-induced UC model, and the relative abundance of gut microbiome changes dynamically in the occurrence and development of ulcerative colitis.
葡聚糖硫酸钠（DSS）诱导的溃疡性结肠炎（UC）动物模型已广泛应用于基础研究，肠道微生物群失调是DSS诱导UC的重要发病机制之一，但其动态变化及与炎症因子的相关性尚不清楚。
将不同浓度DSS诱导的C57BL/6溃疡性结肠炎小鼠模型的临床症状和组织损伤程度与正常小鼠进行比较，最终确定DSS的最佳浓度。然后分析肠道微生物群和炎症因子的测序结果，以确定肠道微生物群的动态模式及其与炎症因子的相关性。
2.5%和3.0%浓度的DSS可导致肠道损伤并诱发结肠炎。然而，3.0%的DSS导致更高的死亡率。此外，DSS诱导的UC模型中肠道微生物群存在动态变化：在毛螺菌属、梭菌属_sensu_stricto_1、毛螺旋菌科_NK4A136_组、未分类_f_未分类_o_梭菌纲_UCG - 014、瘤胃球菌属中，肠道菌群相对丰度先升高后降低，在拟杆菌属、未分类_f_毛螺菌科、柯里杆菌科_UCG - 002中，相对丰度先降低后升高，此外，阿克曼菌属、柯里杆菌科_UCG - 002和嗜黏蛋白阿克曼菌在前14天没有变化，但在第21天显著增加。此外，炎症细胞因子与UC小鼠肠道微生物群失衡密切相关：UC动物模型肠道中的大多数病原菌与促炎因子呈正相关，与抗炎因子呈负相关，而有益菌则相反。
肠道微生态在DSS诱导的UC模型中起重要作用，肠道微生物群的相对丰度在溃疡性结肠炎的发生发展过程中动态变化。
