Emodin Improves Intestinal Health and Immunity through Modulation of Gut Microbiota in Mice Infected by Pathogenic Escherichia coli O(1).
Emodin Improves Intestinal Health and Immunity through Modulation of Gut Microbiota in Mice Infected by Pathogenic Escherichia coli O(1).
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大黄素通过调节致病性大肠杆菌 O1 感染小鼠的肠道微生物群来改善肠道健康和免疫力
DOI：
10.3390/ani11113314
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发表时间：
2021-11-19
期刊：
影响因子：
--
通讯作者：
Zhang J
中科院分区：
文献类型：
--
作者：
Gao R;Wang C;Han A;Tian Y;Ren S;Lv W;Chen A;Zhang J
腹泻与肠道炎症和肠道菌群生态失衡有关。大黄素是一种中草药成分，具有抗菌、抗炎、抗癌等多种药理作用。虽然大黄素的一些特性已被报道，但口服大黄素对肠毒素大肠杆菌(ETEC)感染小鼠肠道微生物群落结构和免疫学参数的影响尚不清楚。因此，本研究旨在探讨大黄素是否通过改变肠道菌群来减轻ETEC感染对小鼠肠道屏障功能和免疫功能的负面影响。结果提示，大黄素可通过增加肠道有益微生物区系的丰度，抑制有害细菌的丰度，从而减轻腹泻，从而减轻O1引起的肠道损伤，改善肠粘膜屏障功能。这项研究的结果将有助于我们了解大黄素是如何通过调节肠道微生物组成来减轻ETEC对肠粘膜屏障损害的影响。摘要观察大黄素对O1诱导的小鼠腹泻模型肠粘膜屏障的影响。成功建立小鼠腹泻模型后，给予药物治疗7天。通过苏木精-伊红染色和高碘酸席夫染色观察肠道病变和杯状细胞的形态和数量，通过RT-PCR、电子显微镜、免疫荧光和16S rRNA测序分析炎症因子、小肠超微结构、MUC-2的表达和肠道微生物区系的变化。结果表明，大黄素可减轻腹泻小鼠肠道的病理损伤。大黄素可降低十二指肠组织中肿瘤坏死因子-α、IL-β、IL-6、MPO和COX-2mRNA水平，增加SIgA、MUC-2水平和杯状细胞数量。微生物组分析表明，大肠杆菌O1降低了细菌丰富度，改变了盲肠内容物中细菌群落在门和目水平的分布格局。值得注意的是，致病性梭状芽胞杆菌和肠杆菌在腹泻小鼠中显著增加。然而，大黄素逆转了这一趋势。因此，大黄素通过增加肠道有益微生物区系的丰度，抑制有害细菌的丰度，从而减轻腹泻，从而保护小鼠的肠道免受大肠杆菌O1的损伤，改善肠粘膜屏障功能。
Simple Summary Diarrhea is associated with intestinal inflammation and ecological imbalance of the intestinal flora. Emodin is an herbal ingredient with various pharmacological effects, such as antibacterial, anti-inflammatory, and anti-cancer. Although several characteristics of emodin have been reported, the effects of orally administered emodin on the structure of the intestinal microbial community and immunological parameters in mice with enterotoxigenic Escherichia coli (ETEC) infection are not well understood. Therefore, this study focused on determining whether emodin mitigates the negative effects of ETEC infection on intestinal barrier function and immune response in mice by altering intestinal flora. The results suggest that emodin protects against intestinal damage induced by E. coli O1 and improves intestinal mucosal barrier function in mice by increasing the abundance of beneficial intestinal microbiota and inhibiting the abundance of harmful bacteria, thereby alleviating diarrhea. The findings of this study will contribute to our understanding of how emodin attenuates the effects of ETEC on intestinal mucosal barrier damage by modulating the microbial composition of the gut. Abstract The effect of emodin on the intestinal mucosal barrier of a mouse E. coli O1-induced diarrhea model was observed. Following successful establishment of a diarrhea model, the mice were treated with drugs for seven days. Intestinal lesions and the shape and the number of goblet cells were assessed via hematoxylin-eosin and periodic-acid-Schiff staining, while changes in inflammatory factors, ultrastructure of the small intestine, expression of MUC-2, and changes in the intestinal microbiota were analyzed via RT-PCR, electron microscopy, immunofluorescence, and 16S rRNA sequencing. Examination showed that emodin ameliorated pathological damage to the intestines of diarrheic mice. RT-PCR indicated that emodin reduced TNF-α, IL-β, IL-6, MPO, and COX-2 mRNA levels in duodenal tissues and increased the levels of sIgA and MUC-2 and the number of goblet cells. Microbiome analysis revealed that Escherichia coli O1 reduced bacterial richness and altered the distribution pattern of bacterial communities at the phylum and order levels in cecum contents. Notably, pathogenic Clostridiales and Enterobacteriales were significantly increased in diarrheic mice. However, emodin reversed the trend. Thus, emodin protected against intestinal damage induced by E. coli O1 and improved intestinal mucosal barrier function in mice by increasing the abundance of beneficial intestinal microbiota and inhibiting the abundance of harmful bacteria, thereby alleviating diarrhea.
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影响因子：
5.9
作者：
Hakansson A;Molin G
通讯作者：
Molin G
用草药配方缓解抗生素相关腹泻期间肠道微生物群的结构调节
DOI：
10.1016/j.ijbiomac.2017.02.060
发表时间：
2017-12-01
影响因子：
8.2
作者：
Lv, Weijie;Liu, Cui;Guo, Shining
通讯作者：
Guo, Shining
影响因子：
3.6
作者：
Andreasen, Anne Sofie;Larsen, Nadja;Pedersen, Bente Klarlund
通讯作者：
Pedersen, Bente Klarlund
DOI：
10.1073/pnas.1219451110
发表时间：
2013-05-28
影响因子：
11.1
作者：
Everard, Amandine;Belzer, Clara;Cani, Patrice D.
通讯作者：
Cani, Patrice D.
影响因子：
2.5
作者：
Becker, Christoph;Neurath, Markus F.;Wirtz, Stefan
通讯作者：
Wirtz, Stefan