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利用遗传学耗尽宿主来源的微生物组分子。

Depletion of microbiome-derived molecules in the host using genetics.

机构信息

Department of Bioengineering and ChEM-H, Stanford University, Stanford, CA 94305, USA.

Jill Roberts Institute for Research in Inflammatory Bowel Disease, Department of Medicine, Weill Cornell Medicine, NY 10021, USA.

出版信息

Science. 2019 Dec 13;366(6471). doi: 10.1126/science.aav1282.

DOI:10.1126/science.aav1282
PMID:31831639
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7141153/
Abstract

The gut microbiota produce hundreds of molecules that are present at high concentrations in the host circulation. Unraveling the contribution of each molecule to host biology remains difficult. We developed a system for constructing clean deletions in spp., the source of many molecules from the gut microbiome. By applying this method to the model commensal organism , we knocked out genes for 10 -derived molecules that accumulate in host tissues. In mice colonized by a for which the production of branched short-chain fatty acids was knocked out, we discovered that these microbial products have immunoglobulin A-modulatory activity.

摘要

肠道微生物群产生数百种分子,这些分子在宿主循环中以高浓度存在。揭示每种分子对宿主生物学的贡献仍然很困难。我们开发了一种在 spp.中构建清洁缺失的系统,该菌是肠道微生物组中许多分子的来源。通过将这种方法应用于模型共生体 ,我们敲除了在宿主组织中积累的 10 种衍生分子的基因。在被敲除支链短链脂肪酸产生的 定植的小鼠中,我们发现这些微生物产物具有调节免疫球蛋白 A 的活性。

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Metabolic, Epigenetic, and Transgenerational Effects of Gut Bacterial Choline Consumption.肠道细菌胆碱摄入的代谢、表观遗传和跨代效应。
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