In inflammatory bowel disease and extraintestinal manifestations: What role does microbiome play?

Q1 Medicine
Yong-Hua Shen , Hao Zhu , Lin Zhou , Yan-Qing Zheng , Zhan Zhang , Ying Xie , Zhen-Qing Liu , Chun-Yan Peng , Lei Wang , Cheng Zhao , Xiao-Qi Zhang
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引用次数: 0

Abstract

Inflammatory bowel disease (IBD) is a systemic disorder affecting intestinal tract and other organs outside the gut, known as extraintestinal manifestations (EIMs). These EIMs are complex and diverse, and early treatment may reduce teratogenic rates and improve quality of life. However, our understanding of EIMs in IBD is currently limited by a lack of mechanistic insight. Fortunately, advances in our understanding of intestinal microecology are allowing us to uncover the underlying mechanisms of EIMs. The gut microbiota can drive aberrant immune activation and intestinal inflammation. Intriguingly, chronic inflammation can also shape the microbiome in reverse and aggravate dysbiosis. Recent research has revealed that microbiome-derived signal molecules play a crucial role in catalyzing enterocolitis and altering mucosal barrier function. Furthermore, gut microbiota-associated antigens can translocate from the intestine to extraintestinal sites, leading to systemic inflammatory responses. The microbiome is showing its potential in treating IBD and EIMs, and microbial engineering approaches, such as probiotic engineering and engineered fecal microbiota transplantation, are exhibiting great promise for IBD therapeutics.

在炎症性肠病和肠外表现中:微生物群起什么作用?
炎症性肠病(IBD)是一种影响肠道和肠道外其他器官的全身性疾病,称为肠外表现(EIMs)。这些eem是复杂和多样的,早期治疗可以降低致畸率,提高生活质量。然而,我们对IBD中的EIMs的理解目前受到缺乏机制洞察力的限制。幸运的是,我们对肠道微生态学的理解的进步使我们能够揭示EIMs的潜在机制。肠道微生物群可以驱动异常的免疫激活和肠道炎症。有趣的是,慢性炎症也可以反向塑造微生物群并加剧生态失调。最近的研究表明,微生物来源的信号分子在催化小肠结肠炎和改变粘膜屏障功能方面起着至关重要的作用。此外,肠道菌群相关抗原可以从肠道转移到肠外,导致全身炎症反应。微生物组在治疗IBD和EIMs方面显示出其潜力,微生物工程方法,如益生菌工程和工程化粪便微生物群移植,在IBD治疗方面显示出巨大的前景。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Engineered regeneration
Engineered regeneration Biomaterials, Medicine and Dentistry (General), Biotechnology, Biomedical Engineering
CiteScore
22.90
自引率
0.00%
发文量
0
审稿时长
33 days
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