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饮食中的果糖和微生物衍生的短链脂肪酸促进肠道共生菌罗伊氏乳杆菌中噬菌体的产生。

Dietary Fructose and Microbiota-Derived Short-Chain Fatty Acids Promote Bacteriophage Production in the Gut Symbiont Lactobacillus reuteri.

机构信息

Department of Food Science, University of Wisconsin-Madison, Madison, WI 53706, USA.

Department of Biochemistry, University of Wisconsin-Madison, Madison, WI 53706, USA.

出版信息

Cell Host Microbe. 2019 Feb 13;25(2):273-284.e6. doi: 10.1016/j.chom.2018.11.016. Epub 2019 Jan 15.

DOI:10.1016/j.chom.2018.11.016
PMID:30658906
Abstract

The mammalian intestinal tract contains a complex microbial ecosystem with many lysogens, which are bacteria containing dormant phages (prophages) inserted within their genomes. Approximately half of intestinal viruses are derived from lysogens, suggesting that these bacteria encounter triggers that promote phage production. We show that prophages of the gut symbiont Lactobacillus reuteri are activated during gastrointestinal transit and that phage production is further increased in response to a fructose-enriched diet. Fructose and exposure to short-chain fatty acids activate the Ack pathway, involved in generating acetic acid, which in turn triggers the bacterial stress response that promotes phage production. L. reuteri mutants of the Ack pathway or RecA, a stress response component, exhibit decreased phage production. Thus, prophages in a gut symbiont can be induced by diet and metabolites affected by diet, which provides a potential mechanistic explanation for the effects of diet on the intestinal phage community.

摘要

哺乳动物肠道中含有一个复杂的微生物生态系统,其中包含许多溶原菌,即细菌基因组内插入了休眠噬菌体(原噬菌体)。大约一半的肠道病毒来源于溶原菌,这表明这些细菌遇到了促进噬菌体产生的触发因素。我们发现,肠道共生菌罗伊氏乳杆菌的原噬菌体在胃肠道转运过程中被激活,而富含果糖的饮食会进一步增加噬菌体的产生。果糖和短链脂肪酸的暴露激活了 Ack 途径,该途径参与生成乙酸,乙酸反过来触发细菌应激反应,促进噬菌体的产生。Ack 途径或应激反应成分 RecA 的缺失突变体的罗伊氏乳杆菌,其噬菌体的产生减少。因此,肠道共生菌中的原噬菌体可以被饮食和受饮食影响的代谢物诱导,这为饮食对肠道噬菌体群落的影响提供了潜在的机制解释。

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