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本文引用的文献

1
Salmonella SPI-1-mediated neutrophil recruitment during enteric colitis is associated with reduction and alteration in intestinal microbiota.肠炎期间沙门氏菌SPI-1介导的中性粒细胞募集与肠道微生物群的减少和改变有关。
Gut Microbes. 2010 Jan;1(1):30-41. doi: 10.4161/gmic.1.1.10950.
2
Gut inflammation provides a respiratory electron acceptor for Salmonella.肠道炎症为沙门氏菌提供呼吸电子受体。
Nature. 2010 Sep 23;467(7314):426-9. doi: 10.1038/nature09415.
3
Enterohaemorrhagic Escherichia coli gains a competitive advantage by using ethanolamine as a nitrogen source in the bovine intestinal content.肠出血性大肠杆菌在牛肠内容物中利用乙醇胺作为氮源获得竞争优势。
Environ Microbiol. 2011 Feb;13(2):365-77. doi: 10.1111/j.1462-2920.2010.02334.x. Epub 2010 Sep 16.
4
A rapid change in virulence gene expression during the transition from the intestinal lumen into tissue promotes systemic dissemination of Salmonella.在从肠道腔转移到组织的过程中,毒力基因表达的快速变化促进了沙门氏菌的全身传播。
PLoS Pathog. 2010 Aug 19;6(8):e1001060. doi: 10.1371/journal.ppat.1001060.
5
Life in the inflamed intestine, Salmonella style.炎症肠道中的沙门氏菌生活方式。
Trends Microbiol. 2009 Nov;17(11):498-506. doi: 10.1016/j.tim.2009.08.008. Epub 2009 Oct 12.
6
Contribution of flagellin pattern recognition to intestinal inflammation during Salmonella enterica serotype typhimurium infection.鞭毛蛋白模式识别在鼠伤寒沙门氏菌感染期间对肠道炎症的作用。
Infect Immun. 2009 May;77(5):1904-16. doi: 10.1128/IAI.01341-08. Epub 2009 Feb 23.
7
Host transmission of Salmonella enterica serovar Typhimurium is controlled by virulence factors and indigenous intestinal microbiota.肠炎沙门氏菌鼠伤寒血清型的宿主传播受毒力因子和肠道固有微生物群控制。
Infect Immun. 2008 Jan;76(1):403-16. doi: 10.1128/IAI.01189-07. Epub 2007 Oct 29.
8
Salmonella enterica serovar typhimurium exploits inflammation to compete with the intestinal microbiota.肠炎沙门氏菌鼠伤寒血清型利用炎症与肠道微生物群竞争。
PLoS Biol. 2007 Oct;5(10):2177-89. doi: 10.1371/journal.pbio.0050244.
9
Robust Salmonella metabolism limits possibilities for new antimicrobials.强大的沙门氏菌新陈代谢限制了新型抗菌药物的研发可能性。
Nature. 2006 Mar 16;440(7082):303-7. doi: 10.1038/nature04616.
10
Salmonella enterica serovar Typhimurium pathogenicity island 2 is necessary for complete virulence in a mouse model of infectious enterocolitis.肠炎沙门氏菌鼠伤寒血清型致病岛2对于感染性小肠结肠炎小鼠模型的完全致病性是必需的。
Infect Immun. 2005 Jun;73(6):3219-27. doi: 10.1128/IAI.73.6.3219-3227.2005.

肠道炎症使沙门氏菌能够利用乙醇胺与微生物组竞争。

Intestinal inflammation allows Salmonella to use ethanolamine to compete with the microbiota.

机构信息

Department of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, CA 95616, USA.

出版信息

Proc Natl Acad Sci U S A. 2011 Oct 18;108(42):17480-5. doi: 10.1073/pnas.1107857108. Epub 2011 Oct 3.

DOI:10.1073/pnas.1107857108
PMID:21969563
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3198331/
Abstract

Conventional wisdom holds that microbes support their growth in vertebrate hosts by exploiting a large variety of nutrients. We show here that use of a specific nutrient (ethanolamine) confers a marked growth advantage on Salmonella enterica serovar Typhimurium (S. Typhimurium) in the lumen of the inflamed intestine. In the anaerobic environment of the gut, ethanolamine supports little or no growth by fermentation. However, S. Typhimurium is able to use this carbon source by inducing the gut to produce a respiratory electron acceptor (tetrathionate), which supports anaerobic growth on ethanolamine. The gut normally converts ambient hydrogen sulfide to thiosulfate, which it then oxidizes further to tetrathionate during inflammation. Evidence is provided that S. Typhimurium's growth advantage in an inflamed gut is because of its ability to respire ethanolamine, which is released from host tissue, but is not utilizable by competing bacteria. By inducing intestinal inflammation, S. Typhimurium sidesteps nutritional competition and gains the ability to use an abundant simple substrate, ethanolamine, which is provided by the host.

摘要

传统观点认为,微生物通过利用大量的营养物质来支持其在脊椎动物宿主中的生长。我们在这里表明,在发炎的肠道腔中,特定营养物质(乙醇胺)的利用赋予了沙门氏菌 Typhimurium(S. Typhimurium)明显的生长优势。在肠道的厌氧环境中,乙醇胺通过发酵几乎或根本无法支持生长。然而,S. Typhimurium 通过诱导肠道产生呼吸电子受体(连四硫酸盐)来利用这种碳源,这支持了乙醇胺的厌氧生长。肠道通常将环境中的硫化氢转化为硫代硫酸盐,然后在炎症期间将其进一步氧化为连四硫酸盐。有证据表明,S. Typhimurium 在发炎肠道中的生长优势是因为它能够呼吸乙醇胺,乙醇胺是从宿主组织中释放出来的,但不能被竞争细菌利用。通过诱导肠道炎症,S. Typhimurium 规避了营养竞争,并获得了使用丰富简单底物乙醇胺的能力,乙醇胺是由宿主提供的。