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本文引用的文献

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ACS Infect Dis. 2023 Aug 11;9(8):1610-1621. doi: 10.1021/acsinfecdis.3c00210. Epub 2023 Jul 26.
2
Fatty Acids Abolish Virulence by Inhibiting Its Master Regulator, VirF.脂肪酸通过抑制其主要调控因子 VirF 来消除毒力。
Microbiol Spectr. 2023 Jun 15;11(3):e0077823. doi: 10.1128/spectrum.00778-23. Epub 2023 May 4.
3
Integrative omics identifies conserved and pathogen-specific responses of sepsis-causing bacteria.整合组学鉴定出导致脓毒症的细菌的保守和病原体特异性反应。
Nat Commun. 2023 Mar 18;14(1):1530. doi: 10.1038/s41467-023-37200-w.
4
Surveying membrane landscapes: a new look at the bacterial cell surface.膜景观调查:细菌细胞表面的新视角。
Nat Rev Microbiol. 2023 Aug;21(8):502-518. doi: 10.1038/s41579-023-00862-w. Epub 2023 Feb 24.
5
Characterizing the role of phosphatidylglycerol-phosphate phosphatases in cell envelope biogenesis and antibiotic resistance.表征磷脂酰甘油磷酸磷酸酶在细胞膜生物合成和抗生素抗性中的作用。
Cell Surf. 2022 Dec 10;9:100092. doi: 10.1016/j.tcsw.2022.100092. eCollection 2023 Dec.
6
Simulated Docking Predicts Putative Channels for the Transport of Long-Chain Fatty Acids in .模拟对接预测长链脂肪酸跨膜转运的潜在通道。
Biomolecules. 2022 Sep 9;12(9):1269. doi: 10.3390/biom12091269.
7
Identification of the Shigella flexneri Wzy Domain Modulating Wzz Interaction and Detection of the Wzy/Wzz/Oag Complex.鉴定志贺氏菌 Wzy 结构域调节 Wzz 相互作用并检测 Wzy/Wzz/Oag 复合物。
J Bacteriol. 2022 Sep 20;204(9):e0022422. doi: 10.1128/jb.00224-22. Epub 2022 Aug 18.
8
Dietary Fatty Acid Intake and the Colonic Gut Microbiota in Humans.膳食脂肪酸摄入与人类结肠肠道微生物群。
Nutrients. 2022 Jun 29;14(13):2722. doi: 10.3390/nu14132722.
9
Detection of a disulphide bond and conformational changes in Shigella flexneri Wzy, and the role of cysteine residues in polymerase activity.检测志贺氏菌 flexneri Wzy 中的二硫键和构象变化,以及半胱氨酸残基在聚合酶活性中的作用。
Biochim Biophys Acta Biomembr. 2022 May 1;1864(5):183871. doi: 10.1016/j.bbamem.2022.183871. Epub 2022 Jan 26.
10
The human bile salt sodium deoxycholate induces metabolic and cell envelope changes in Typhi leading to bile resistance.人胆汁盐脱氧胆酸钠诱导 Typhi 发生代谢和细胞包膜变化,导致其对胆汁产生耐药性。
J Med Microbiol. 2022 Jan;71(1). doi: 10.1099/jmm.0.001461.

感染过程中宿主脂质的重塑和消耗。

remodeling and consumption of host lipids during infection.

机构信息

Department of Molecular and Biomedical Science, School of Biological Sciences, Research Centre for Infectious Diseases, University of Adelaide, Adelaide, Australia.

Molecular Sciences and Technology, College of Science and Engineering, Flinders University, Adelaide, Australia.

出版信息

J Bacteriol. 2023 Dec 19;205(12):e0032023. doi: 10.1128/jb.00320-23. Epub 2023 Nov 22.

DOI:10.1128/jb.00320-23
PMID:37991380
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10729657/
Abstract

Bacterial pathogens have vastly distinct sites that they inhabit during infection. This requires adaptation due to changes in nutrient availability and antimicrobial stress. The bacterial surface is a primary barrier, and here, we show that the bacterial pathogen increases its surface decorations when it transitions to an intracellular lifestyle. We also observed changes in bacterial and host cell fatty acid homeostasis. Specifically, intracellular increased the expression of their fatty acid degradation pathway, while the host cell lipid pool was significantly depleted. Importantly, bacterial proliferation could be inhibited by fatty acid supplementation of host cells, thereby providing novel insights into the possible link between human malnutrition and susceptibility to .

摘要

细菌病原体在感染过程中栖息在截然不同的部位。这需要适应,因为营养物质的可用性和抗菌应激会发生变化。细菌表面是主要的屏障,在这里,我们发现当细菌病原体转变为细胞内生活方式时,它会增加其表面装饰物。我们还观察到细菌和宿主细胞脂肪酸动态平衡的变化。具体来说,细胞内的细菌增加了其脂肪酸降解途径的表达,而宿主细胞的脂质库则明显减少。重要的是,通过向宿主细胞补充脂肪酸可以抑制细菌的增殖,从而为人类营养不良与易感性之间的可能联系提供新的见解。