Department of Gastroenterology and Hepatology, Guangzhou Digestive Disease Center, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, No. 1 Panfu Road, Guangzhou, 510180, China.
Department of Geriatrics, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, 510180, China.
BMC Microbiol. 2021 Oct 16;21(1):279. doi: 10.1186/s12866-021-02342-8.
Dextran sulfate sodium (DSS) replicates ulcerative colitis (UC)-like colitis in murine models. However, the microbial characteristics of DSS-triggered colitis require further clarification. To analyze the changes in gut microbiota associated with DSS-induced acute and chronic colitis.
Acute colitis was induced in mice by administering 3% DSS for 1 week in the drinking water, and chronic colitis was induced by supplementing drinking water with 2.5% DSS every other week for 5 weeks. Control groups received the same drinking water without DSS supplementation. The histopathological score and length of the colons, and disease activity index (DAI) were evaluated to confirm the presence of experimental colitis. Intestinal microbiota was profiled by 16S rDNA sequencing of cecal content.
Mice with both acute and chronic DSS-triggered colitis had significantly higher DAI and colon histopathological scores in contrast to the control groups (P < 0.0001, P < 0.0001), and the colon was remarkably shortened (P < 0.0001, P < 0.0001). The gut microbiota α-diversity was partly downregulated in both acute and chronic colitis groups in contrast to their respective control groups (Pielou index P = 0.0022, P = 0.0649; Shannon index P = 0.0022, P = 0.0931). The reduction in the Pielou and Shannon indices were more obvious in mice with acute colitis (P = 0.0022, P = 0.0043). The relative abundance of Bacteroides and Turicibacter was increased (all P < 0.05), while that of Lachnospiraceae, Ruminococcaceae, Ruminiclostridium, Rikenella, Alistipes, Alloprevotella, and Butyricicoccus was significantly decreased after acute DSS induction (all P < 0.05). The relative abundance of Bacteroides, Akkermansia, Helicobacter, Parabacteroides, Erysipelatoclostridium, Turicibacter and Romboutsia was also markedly increased (all P < 0.05), and that of Lachnospiraceae_NK4A136_group, Alistipes, Enterorhabdus, Prevotellaceae_UCG-001, Butyricicoccus, Ruminiclostridium_6, Muribaculum, Ruminococcaceae_NK4A214_group, Family_XIII_UCG-001 and Flavonifractor was significantly decreased after chronic DSS induction (all P < 0.05).
DSS-induced acute and chronic colitis demonstrated similar symptoms and histopathological changes. The changes in the gut microbiota of the acute colitis model were closer to that observed in UC. The acute colitis model had greater abundance of SCFAs-producing bacteria and lower α-diversity compared to the chronic colitis model.
硫酸葡聚糖钠（DSS）在小鼠模型中复制溃疡性结肠炎（UC）样结肠炎。然而，DSS 引发的结肠炎的微生物特征需要进一步阐明。分析与 DSS 诱导的急性和慢性结肠炎相关的肠道微生物群变化。
通过在饮用水中添加 3%的 DSS 1 周来诱导小鼠急性结肠炎，通过每隔一周在饮用水中添加 2.5%的 DSS 5 周来诱导慢性结肠炎。对照组接受相同的不含 DSS 补充的饮用水。通过对盲肠内容物进行 16S rDNA 测序来分析肠道微生物群。
与对照组相比，具有急性和慢性 DSS 触发的结肠炎的小鼠的 DAI 和结肠组织病理学评分明显更高（P < 0.0001，P < 0.0001），并且结肠明显缩短（P < 0.0001，P < 0.0001）。与各自的对照组相比，急性和慢性结肠炎组的肠道微生物群 α-多样性部分下调（Pielou 指数 P = 0.0022，P = 0.0649；Shannon 指数 P = 0.0022，P = 0.0931）。急性结肠炎小鼠的 Pielou 和 Shannon 指数下降更为明显（P = 0.0022，P = 0.0043）。拟杆菌属和 Turicibacter 的相对丰度增加（均 P < 0.05），而lachnospiraceae、Ruminococcaceae、Ruminiclostridium、Rikenella、Alistipes、Alloprevotella 和 Butyricicoccus 的相对丰度在急性 DSS 诱导后显著降低（均 P < 0.05）。Bacteroides、Akkermansia、Helicobacter、Parabacteroides、Erysipelatoclostridium、Turicibacter 和 Romboutsia 的相对丰度也明显增加（均 P < 0.05），而lachnospiraceae_NK4A136_group、Alistipes、Enterorhabdus、Prevotellaceae_UCG-001、Butyricicoccus、Ruminiclostridium_6、Muribaculum、Ruminococcaceae_NK4A214_group、Family_XIII_UCG-001 和 Flavonifractor 的相对丰度在慢性 DSS 诱导后显著降低（均 P < 0.05）。
DSS 诱导的急性和慢性结肠炎表现出相似的症状和组织病理学变化。急性结肠炎模型中肠道微生物群的变化更接近 UC 中观察到的变化。与慢性结肠炎模型相比，急性结肠炎模型中 SCFA 产生菌的丰度更高，α-多样性更低。
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