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头孢他啶耐药的代谢机制 （原文表述不完整，缺少具体研究对象等关键信息）

Metabolic mechanism of ceftazidime resistance in .

作者信息

Liu Shi-Rao, Peng Xuan-Xian, Li Hui

机构信息

Center for Proteomics and Metabolomics, State Key Laboratory of Biocontrol, Guangdong Province Key Laboratory for Pharmaceutical Functional Genes, School of Life Sciences, Sun Yat-sen University, University City, Guangzhou 510006, People's Republic of China,

Laboratory for Marine Fisheries Science and Food Production Processes, Qingdao National Laboratory for Marine Science and Technology, Qingdao 266071, People's Republic of China,

出版信息

Infect Drug Resist. 2019 Feb 13;12:417-429. doi: 10.2147/IDR.S179639. eCollection 2019.

DOI:10.2147/IDR.S179639
PMID:30863124
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6388739/
Abstract

BACKGROUND

Microbial metabolism confounds antibiotic efficacy. However, information regarding effect of metabolism on cephalosporin antibiotics-mediated killing and is largely absence, although the drugs are widely used in clinic and the bacteria are pathogens to both human and aquaculture animals.

PURPOSE

This study explores the metabolome of cephalosporin antibiotic-resistant and analyzes the role of bacterial metabolism in drug and multidrug-resistance.

RESULTS

The metabolomes of isogenic ceftazidime-resistant (VA-R) and ceftazidime-sensitive (VA-S) were analyzed using gas chromatography -mass spectrometry. The metabolome of VA-R is characterized by inefficient respiration, an inefficient pyruvate cycle (P cycle), increased biosynthesis of fatty acids and decreased membrane proton motive force. This hypothesis was confirmed by the fact that furfural and malonate, inhibitors of pyruvate dehydrogenase and succinate dehydrogenase (P cycle enzymes), respectively, increased resistance of VA-R to antibiotics, while exposure to triclosan, to inhibit biosynthesis of fatty acids, decreased resistance.

CONCLUSION

These results contribute to our understanding of mechanisms of bacterial antibiotic-resistance and may lead to more effective approaches to treat, manage or prevent infections caused by antibiotic-resistant pathogens including those of the species.

摘要

背景

微生物代谢会影响抗生素疗效。然而，尽管头孢菌素类抗生素在临床上广泛使用，且这些细菌对人类和水产养殖动物均为病原体，但关于代谢对头孢菌素类抗生素介导的杀菌作用的影响的信息却基本缺失。

目的

本研究探索头孢菌素类抗生素耐药性[细菌名称]的代谢组，并分析细菌代谢在药物及多重耐药中的作用。

结果

使用气相色谱-质谱联用技术分析了同源的对头孢他啶耐药的细菌名称和对头孢他啶敏感的细菌名称的代谢组。VA-R的代谢组特征为呼吸效率低下、丙酮酸循环（P循环）效率低下、脂肪酸生物合成增加以及膜质子动力降低。这一假设通过以下事实得到证实：分别作为丙酮酸脱氢酶和琥珀酸脱氢酶（P循环酶）抑制剂的糠醛和丙二酸，增加了VA-R对抗生素的耐药性，而暴露于三氯生以抑制脂肪酸生物合成时，则降低了耐药性。

结论

这些结果有助于我们理解细菌抗生素耐药机制，并可能带来更有效的方法来治疗、管理或预防由包括[细菌名称]在内的抗生素耐药病原体引起的感染。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0246/6388739/17dacd4158df/idr-12-417Fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0246/6388739/08be1551d9ec/idr-12-417Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0246/6388739/52b39b59beab/idr-12-417Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0246/6388739/56878f53ac2d/idr-12-417Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0246/6388739/162f329fe6a2/idr-12-417Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0246/6388739/32e7ba550733/idr-12-417Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0246/6388739/16d0d3113326/idr-12-417Fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0246/6388739/0bbdf750da7f/idr-12-417Fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0246/6388739/17dacd4158df/idr-12-417Fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0246/6388739/08be1551d9ec/idr-12-417Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0246/6388739/52b39b59beab/idr-12-417Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0246/6388739/56878f53ac2d/idr-12-417Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0246/6388739/162f329fe6a2/idr-12-417Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0246/6388739/32e7ba550733/idr-12-417Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0246/6388739/16d0d3113326/idr-12-417Fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0246/6388739/0bbdf750da7f/idr-12-417Fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0246/6388739/17dacd4158df/idr-12-417Fig8.jpg

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