Tissue metabolism and host-microbial interactions in the intestinal mucosa.

Tissue metabolism and host-microbial interactions in the intestinal mucosa.
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DOI:
10.1016/j.freeradbiomed.2016.09.027
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发表时间:
2017-04
影响因子:
7.4
通讯作者:
Colgan SP
Colgan SP
中科院分区:
医学1区
文献类型:
--
作者:
Chun C;Zheng L;Colgan SP

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近年来,在胃肠道(GI)粘膜的研究已经教会了我们一些重要的经验教训有关的组织氧合和代谢的健康和疾病。高度血管化的粘膜紧邻含有数万亿代谢活性微生物(即微生物组)的厌氧腔,这导致体内更严峻的组织微环境之一。这些研究还暗示了氧代谢和缺氧在炎症中的突出作用,所谓的“炎性缺氧”,其由多种耗氧酶的激活引起。微生物组和微生物衍生代谢物组成的炎症相关变化揭示了转录因子缺氧诱导因子(HIF)在调节促进炎症消退的关键靶基因中的重要作用。对这些通路的分析为理解稳态和疾病的基本机制提供了大量机会,并确定了新的干预目标。在这里,我们回顾了最近的进展,我们的理解代谢的影响宿主微生物的相互作用在胃肠道粘膜。
In recent years, studies in the gastrointestinal (GI) mucosa have taught us a number of important lessons related to tissue oxygenation and metabolism in health and disease. The highly vascularized mucosa lies immediately adjacent to an anaerobic lumen containing trillions of metabolically active microbes (i.e. the microbiome) that results in one of the more austere tissue microenvironments in the body. These studies have also implicated a prominent role for oxygen metabolism and hypoxia in inflammation, so called “inflammatory hypoxia”, that results from the activation of multiple oxygen consuming enzymes. Inflammation-associated shifts in the composition of the microbiome and microbial-derived metabolites have revealed a prominent role for the transcription factor hypoxia-inducible factor (HIF) in the regulation of key target genes that promote inflammatory resolution. Analyses of these pathways have provided a multitude of opportunities for understanding basic mechanisms of both homeostasis and disease and have defined new targets for intervention. Here, we review recent advances in our understanding of metabolic influences on host-microbe interactions in the GI mucosa.
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