Vibrio alginolyticus Survives From Ofloxacin Stress by Metabolic Adjustment.
Vibrio alginolyticus Survives From Ofloxacin Stress by Metabolic Adjustment.
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溶藻弧菌通过代谢调节从氧氟沙星应激中存活下来
DOI：
10.3389/fmicb.2022.818923
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发表时间：
2022
影响因子：
5.2
通讯作者：
Peng B
中科院分区：
文献类型：
--
作者：
Yin Y;Yin Y;Yang H;Chen Z;Zheng J;Peng B
耐抗生素的溶藻弧菌成为了一个全球性挑战，威胁着人类健康和食品安全。尽管人们已对其抗生素耐药机制展开广泛研究，但应对这类感染的方法却基本缺失。已有研究表明，代谢调节是提高抗生素疗效的一种新途径。在本研究中，我们对暴露于0.3或0.5微克/毫升氧氟沙星（OFX）的溶藻弧菌的代谢特征进行了表征。通过代谢组分析，我们发现用这两种不同浓度的OFX处理的细菌产生了不同的代谢特征。虽然部分代谢产物在两组中都存在，但其他代谢产物则代表了各自的特征。通路富集分析表明，与0.5微克/毫升OFX处理的细菌相比，0.3微克/毫升OFX处理的细菌中丙酮酸循环受到破坏。重要的是，丙酮酸循环的破坏赋予了细菌在0.5微克/毫升抗生素压力下生存的能力。进一步分析发现，0.3微克/毫升OFX处理的细菌中脂肪酸生物合成增强，而抑制脂肪酸合成则完全阻止了细菌在这种剂量的抗生素压力下存活。我们的研究表明，细菌通过调节代谢通量来适应抗生素压力以存活，这一机制可作为提高抗生素疗效的靶点。
Antibiotic-resistant Vibrio alginolyticus becomes a worldwide challenge threatening both human health and food safety. The approach in managing such infection is largely absent, despite the fact that the mechanisms of antibiotic resistance have been extensively investigated. Metabolic modulation has been documented to be a novel approach in improving antibiotic efficacy. In this study, we characterize the metabolic signature of V. alginolyticus exposed to 0.3 or 0.5 μg/ml of ofloxacin (OFX). By profiling the metabolome, we find that bacteria treated by the two different concentrations of OFX generate different metabolic signatures. While a part of these metabolites was shared by both groups, the other metabolites represent their own signatures. The pathway enrichment analysis demonstrates that the pyruvate cycle is disrupted in the bacteria treated by the 0.3 μg/ml OFX as compared to those by the 0.5 μg/ml. Importantly, the disruption of pyruvate cycle confers the capability of bacteria to survive under 0.5 μg/ml of antibiotic stress. Further analysis identifies that the fatty acid biosynthesis is elevated in bacteria treated by 0.3 μg/ml OFX, and inhibition on fatty acid completely prevents the bacteria from survival even under such dose of antibiotic stress. Our study suggests that bacteria adapt to antibiotic stress by modulating the metabolic flux for survival, which could be targeted to increase antibiotic efficacy.
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