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饮食诱导的宿主-微生物相互作用:改善炎症性肠病的个性化饮食策略

Diet-Induced Host-Microbe Interactions: Personalized Diet Strategies for Improving Inflammatory Bowel Disease.

作者信息

Lee Jae-Eun, Kim Kyoung Su, Koh Hong, Lee Dong-Woo, Kang Nam Joo

机构信息

School of Food Science and Biotechnology, Kyungpook National University, Daegu, South Korea.

Department of Biotechnology, Yonsei University, Seoul, South Korea.

出版信息

Curr Dev Nutr. 2022 Jun 25;6(8):nzac110. doi: 10.1093/cdn/nzac110. eCollection 2022 Aug.

DOI:10.1093/cdn/nzac110
PMID:36060223
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9429970/
Abstract

Inflammatory bowel disease (IBD) is an idiopathic inflammatory disease. Environmental sanitization, modern lifestyles, advanced medicines, ethnic origins, host genetics and immune systems, mucosal barrier function, and the gut microbiota have been delineated to explain how they cause mucosal inflammation. However, the pathogenesis of IBD and its therapeutic targets remain elusive. Recent studies have highlighted the importance of the human gut microbiota in health and disease, suggesting that the pathogenesis of IBD is highly associated with imbalances of the gut microbiota or alterations of epithelial barrier function in the gastrointestinal (GI) tract. Moreover, diet-induced alterations of the gut microbiota in the GI tract modulate immune responses and perturb metabolic homeostasis. This review summarizes recent findings on IBD and its association with diet-induced changes in the gut microbiota; furthermore, it discusses how diets can modulate host gut microbes and immune systems, potentiating the impact of personalized diets on therapeutic targets for IBD.

摘要

炎症性肠病(IBD)是一种特发性炎症性疾病。环境卫生、现代生活方式、先进药物、种族起源、宿主遗传学和免疫系统、黏膜屏障功能以及肠道微生物群已被阐述,以解释它们如何引发黏膜炎症。然而,IBD的发病机制及其治疗靶点仍然难以捉摸。最近的研究强调了人类肠道微生物群在健康和疾病中的重要性,表明IBD的发病机制与肠道微生物群失衡或胃肠道(GI)上皮屏障功能改变高度相关。此外,饮食引起的胃肠道肠道微生物群改变会调节免疫反应并扰乱代谢稳态。本综述总结了关于IBD及其与饮食引起的肠道微生物群变化之间关联的最新发现;此外,还讨论了饮食如何调节宿主肠道微生物和免疫系统,增强个性化饮食对IBD治疗靶点的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc11/9429970/5829525627ca/nzac110fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc11/9429970/db60301cd4a2/nzac110fig1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc11/9429970/ba0b9decfc94/nzac110fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc11/9429970/b7f1950c25f8/nzac110fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc11/9429970/7ad28977234f/nzac110fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc11/9429970/5829525627ca/nzac110fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc11/9429970/db60301cd4a2/nzac110fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc11/9429970/a18b39865239/nzac110fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc11/9429970/ba0b9decfc94/nzac110fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc11/9429970/b7f1950c25f8/nzac110fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc11/9429970/7ad28977234f/nzac110fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc11/9429970/5829525627ca/nzac110fig6.jpg

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