The contribution of gut bacterial metabolites in the human immune signaling pathway of non-communicable diseases.
The contribution of gut bacterial metabolites in the human immune signaling pathway of non-communicable diseases.
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DOI：
10.1080/19490976.2021.1882927
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发表时间：
2021-01
期刊：
影响因子：
12.2
通讯作者：
Hankemeier T
中科院分区：
文献类型：
--
作者：
Hosseinkhani F;Heinken A;Thiele I;Lindenburg PW;Harms AC;Hankemeier T
肠道微生物群与其宿主之间的相互作用紊乱已在不同的非传染性疾病（NCDs）中得到证实，如代谢综合征、神经退行性疾病和自身免疫性疾病。这些改变的相互作用大多数是通过肠道微生物群和宿主免疫系统之间的代谢串扰产生的，诱发了所有非传染性疾病特征的低度慢性炎症。在这篇综述中，我们讨论了细菌代谢物对非传染性疾病免疫信号通路的贡献。然后，我们回顾了有助于合理设计微生物疗法的最新进展。利用基于代谢组学的系统生物学平台对宿主和肠道微生物群代谢之间的这些交叉点进行更深入的了解，有望揭示驱动代谢易感性的基本机制，并为利用微生物治疗机会治疗和预防非传染性疾病提供新的途径。缩写：NCDs：非传染性疾病，IBD：炎症性肠病，IL：白细胞介素，T2D: 2型糖尿病，SCFAs：短链脂肪酸，HDAC：组蛋白去乙酰化酶，GPCR: g蛋白偶联受体，5-HT: 5-羟色胺受体信号传导，DCs：树突状细胞，IECs：肠上皮细胞，T-reg: T调节细胞，NF-κB：核因子κB， TNF-α：肿瘤坏死因子α， Th: T辅助细胞，CNS：中枢神经系统，ECs：肠色素细胞，非甾体抗炎药。非甾体类抗炎药物，AhR：芳烃受体，IDO：吲哚胺2,3-双加氧酶，QUIN：喹啉酸，PC：磷脂酰胆碱，TMA：三甲胺，TMAO：三甲胺n-氧化物，CVD：心血管疾病，NASH：非酒精性脂肪性肝炎，BAs：胆汁酸，FXR：法尼松X受体，CDCA：鹅去氧胆酸，DCA：去氧胆酸，LCA：石胆酸，UDCA：熊去氧胆酸，CB：大麻素受体，COBRA：约束重构与分析
The interaction disorder between gut microbiota and its host has been documented in different non-communicable diseases (NCDs) such as metabolic syndrome, neurodegenerative disease, and autoimmune disease. The majority of these altered interactions arise through metabolic cross-talk between gut microbiota and host immune system, inducing a low-grade chronic inflammation that characterizes all NCDs. In this review, we discuss the contribution of bacterial metabolites to immune signaling pathways involved in NCDs. We then review recent advances that aid to rationally design microbial therapeutics. A deeper understanding of these intersections between host and gut microbiota metabolism using metabolomics-based system biology platform promises to reveal the fundamental mechanisms that drive metabolic predispositions to disease and suggest new avenues to use microbial therapeutic opportunities for NCDs treatment and prevention. Abbreviations: NCDs: non-communicable disease, IBD: inflammatory bowel disease, IL: interleukin, T2D: type 2 diabetes, SCFAs: short-chain fatty acids, HDAC: histone deacetylases, GPCR: G-protein coupled receptors, 5-HT: 5-hydroxytryptamine receptor signaling, DCs: dendritic cells, IECs: intestinal epithelial cells, T-reg: T regulatory cell, NF-κB: nuclear factor κB, TNF-α: tumor necrosis factor alpha, Th: T helper cell, CNS: central nervous system, ECs: enterochromaffin cells, NSAIDs: non-steroidal anti-inflammatory drugs, AhR: aryl hydrocarbon receptor, IDO: indoleamine 2,3-dioxygenase, QUIN: quinolinic acid, PC: phosphatidylcholine, TMA: trimethylamine, TMAO: trimethylamine N-oxide, CVD: cardiovascular disease, NASH: nonalcoholic steatohepatitis, BAs: bile acids, FXR: farnesoid X receptor, CDCA: chenodeoxycholic acid, DCA: deoxycholic acid, LCA: lithocholic acid, UDCA: ursodeoxycholic acid, CB: cannabinoid receptor, COBRA: constraint-based reconstruction and analysis
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DOI：
10.1126/science.1198469
发表时间：
2011-01-21
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Atarashi K;Tanoue T;Shima T;Imaoka A;Kuwahara T;Momose Y;Cheng G;Yamasaki S;Saito T;Ohba Y;Taniguchi T;Takeda K;Hori S;Ivanov II;Umesaki Y;Itoh K;Honda K
通讯作者：
Honda K
DOI：
10.1038/s41568-018-0050-3
发表时间：
2018-11
期刊：
Nature reviews. Cancer
影响因子：
--
作者：
Casero RA Jr;Murray Stewart T;Pegg AE
通讯作者：
Pegg AE
DOI：
10.1038/ijo.2015.84
发表时间：
2015-09
期刊：
International journal of obesity (2005)
影响因子：
--
作者：
Byrne CS;Chambers ES;Morrison DJ;Frost G
通讯作者：
Frost G
影响因子：
3.5
作者：
Aguilera, M.;Vergara, P.;Martinez, V.
通讯作者：
Martinez, V.
从宏基因组数据到硅微生物群中个性化：预测克罗恩病的饮食补充剂。
影响因子：
4
作者：
Bauer E;Thiele I
通讯作者：
Thiele I