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母体食用发酵饮食通过调节肠道微生物群来保护后代免受肠道炎症的影响。

Maternal consumption of a fermented diet protects offspring against intestinal inflammation by regulating the gut microbiota.

机构信息

National Engineering Laboratory for Feed Safety and Pollution Prevention and Controlling; Key Laboratory of Molecular Animal Nutrition, Ministry of Education; Key Laboratory of Animal Nutrition and Feed Science (Eastern of China), Ministry of Agriculture and Rural Affairs; Key Laboratory of Animal Feed and Nutrition of Zhejiang Province; Institute of Feed Science, Zhejiang University, 866 Yuhang Tang Road, Hangzhou, 310058, PR China.

出版信息

Gut Microbes. 2022 Jan-Dec;14(1):2057779. doi: 10.1080/19490976.2022.2057779.

DOI:10.1080/19490976.2022.2057779
PMID:35506256
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9090288/
Abstract

The neonatal intestinal tract is immature and can be easily infected by pathogens causing inflammation. Maternal diet manipulation is a promising nutritional strategy to enhance the gut health of offspring. A fermented diet is a gut microbiota targeting diet containing live probiotics and their metabolites, which benefit the gut and overall health host. However, it remains unclear how a maternal fermented diet (MFD) affects neonatal intestinal inflammation. Here, and models together with multi-omics analysis were applied to investigate the impacts and the underlying mechanism through which an MFD prevents from gut inflammation in neonates. An MFD remarkably improved the performance of both sows and piglets and significantly altered the gut microbiome and milk metabolome of sows. In addition, the MFD significantly accelerated the maturation of the gut microbiota of neonates and increased the abundance of gut and the microbial functions of amino acid-related enzymes and glucose metabolism on the weaning day. Notably, the MFD reduced susceptibility to colonic inflammation in offspring. The fecal microbiota of sows was then transplanted into mouse dams and it was found that the mouse dams and pups in the MFD group alleviated the LPS-induced decrease in gut abundance and barrier injury. Milk L-glutamine (GLN) and gut (LR) were found as two of the main MFD-induced sow effectors that contributed to the gut health of piglets. The properties of LR and GLN in modulating gut microbiota and alleviating colonic inflammation by inhibiting the phosphorylation of p38 and JNK and activation of Caspase 3 were further verified. These findings provide the first data revealing that an MFD drives neonate gut microbiota development and ameliorates the colonic inflammation by regulating the gut microbiota. This fundamental evidence might provide references for modulating maternal nutrition to enhance early-life gut health and prevent gut inflammation.

摘要

新生动物的肠道尚未成熟,容易受到病原体感染,引发炎症。通过调整母体饮食来干预新生动物的肠道发育是一种有前景的营养策略,可以促进其肠道健康。发酵饮食是一种靶向肠道微生物群的饮食,其中含有活益生菌及其代谢物,对肠道和宿主整体健康有益。然而,目前尚不清楚母体发酵饮食(MFD)如何影响新生动物的肠道炎症。在这里,我们采用 和 模型并结合多组学分析,研究了 MFD 预防新生动物肠道炎症的作用及其潜在机制。MFD 显著改善了母猪和仔猪的生产性能,并显著改变了母猪的肠道微生物群和乳汁代谢组。此外,MFD 显著加速了新生动物肠道微生物群的成熟,并增加了肠道 丰度和与氨基酸相关的酶和葡萄糖代谢的微生物功能,这一过程在断奶日达到顶峰。值得注意的是,MFD 降低了新生动物对结肠炎症的易感性。随后将母猪粪便微生物群移植到母鼠体内,发现 MFD 组的母鼠及其幼崽减轻了 LPS 诱导的肠道 丰度降低和屏障损伤。结果表明,MFD 诱导产生的两种主要的母猪效应物——乳 L-谷氨酰胺(GLN)和肠道 (LR),对仔猪的肠道健康有贡献。LR 和 GLN 通过抑制 p38 和 JNK 的磷酸化以及激活 Caspase 3,调节肠道微生物群并缓解结肠炎症的特性得到了进一步验证。这些发现为首次揭示 MFD 通过调节肠道微生物群来促进新生动物肠道微生物群发育并改善结肠炎症提供了数据支持。这些基础性的证据可能为通过调节母体营养来增强早期生命的肠道健康和预防肠道炎症提供参考。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cf5/9090288/faf7e6b807c1/KGMI_A_2057779_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cf5/9090288/8c8bc6915525/KGMI_A_2057779_UF0001_OC.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cf5/9090288/cbc8b58106d5/KGMI_A_2057779_F0003_OC.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cf5/9090288/d9f45fbbb647/KGMI_A_2057779_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cf5/9090288/060133a1dced/KGMI_A_2057779_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cf5/9090288/3cbc5b984493/KGMI_A_2057779_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cf5/9090288/faf7e6b807c1/KGMI_A_2057779_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cf5/9090288/8c8bc6915525/KGMI_A_2057779_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cf5/9090288/1c3517c10189/KGMI_A_2057779_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cf5/9090288/4b333b5a5be5/KGMI_A_2057779_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cf5/9090288/cbc8b58106d5/KGMI_A_2057779_F0003_OC.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cf5/9090288/060133a1dced/KGMI_A_2057779_F0006_OC.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cf5/9090288/faf7e6b807c1/KGMI_A_2057779_F0008_OC.jpg

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