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微生物群衍生的1,2-丙二醇的呼吸作用在结肠炎期间推动沙门氏菌扩张。

Respiration of Microbiota-Derived 1,2-propanediol Drives Salmonella Expansion during Colitis.

作者信息

Faber Franziska, Thiennimitr Parameth, Spiga Luisella, Byndloss Mariana X, Litvak Yael, Lawhon Sara, Andrews-Polymenis Helene L, Winter Sebastian E, Bäumler Andreas J

机构信息

Department of Medial Microbiology and Immunology, School of Medicine, University of California Davis, Davis, CA, United States of America.

Department of Microbiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.

出版信息

PLoS Pathog. 2017 Jan 5;13(1):e1006129. doi: 10.1371/journal.ppat.1006129. eCollection 2017 Jan.

Abstract

Intestinal inflammation caused by Salmonella enterica serovar Typhimurium increases the availability of electron acceptors that fuel a respiratory growth of the pathogen in the intestinal lumen. Here we show that one of the carbon sources driving this respiratory expansion in the mouse model is 1,2-propanediol, a microbial fermentation product. 1,2-propanediol utilization required intestinal inflammation induced by virulence factors of the pathogen. S. Typhimurium used both aerobic and anaerobic respiration to consume 1,2-propanediol and expand in the murine large intestine. 1,2-propanediol-utilization did not confer a benefit in germ-free mice, but the pdu genes conferred a fitness advantage upon S. Typhimurium in mice mono-associated with Bacteroides fragilis or Bacteroides thetaiotaomicron. Collectively, our data suggest that intestinal inflammation enables S. Typhimurium to sidestep nutritional competition by respiring a microbiota-derived fermentation product.

摘要

肠炎沙门氏菌鼠伤寒血清型引起的肠道炎症增加了电子受体的可用性,这些电子受体为病原体在肠腔内的呼吸生长提供能量。在此我们表明,在小鼠模型中驱动这种呼吸扩展的碳源之一是1,2 - 丙二醇,一种微生物发酵产物。利用1,2 - 丙二醇需要由病原体的毒力因子诱导的肠道炎症。鼠伤寒沙门氏菌利用有氧呼吸和无氧呼吸来消耗1,2 - 丙二醇并在小鼠大肠中增殖。在无菌小鼠中,利用1,2 - 丙二醇并没有带来益处,但pdu基因赋予了鼠伤寒沙门氏菌在与脆弱拟杆菌或嗜热栖热放线菌单联的小鼠中的适应性优势。总体而言,我们的数据表明,肠道炎症使鼠伤寒沙门氏菌能够通过呼吸微生物群衍生的发酵产物来避开营养竞争。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/48ea/5215881/e6fc3d0f5101/ppat.1006129.g001.jpg

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