Abstract
Enterobacter cloacae is an opportunistic pathogen widely distributed in human and animal intestinal systems. The secretion of extended-spectrum β-lactamases (ESBLs) and cephalosporinase (AmpC) endows E. cloacae with strong drug resistance. In a previous study by our group, protein expression of E. cloacae under phoxim stress was measured by two-dimensional electrophoresis. Here, nuclear magnetic resonance was used to detect differences in E. cloacae metabonomics when under phoxim stress. We determined that there are 29 types of metabolites that differ between phoxim stress and normal culture conditions. Among these, 6 types of metabolites were upregulated in the phoxim stress group, and 23 types of metabolites were inhibited. Though enrichment analysis, seven pathways were identified by different expression levels of metabolites, which were involved in DNA and RNA synthesis, DNA damage repair, antioxidation and functions of the cell membrane and cell wall. The mechanism underlying how phoxim affects E. cloacae was determined by studying the results of both two-dimensional electrophoresis in our prior work and the analysis of E. cloacae metabonomic changes under phoxim stress.
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Acknowledgements
This work was supported by the Public Science and Technology Research Funds ocean projects (201105007, 201005016), Ningbo ocean economic innovation and development of regional demonstration projects (Research and demonstration of key technology on marine bacteria detection of gene chip industrialization),the National Natural Science Foundation of China (41306135), the Donghai sea collaborative innovation center for industrial upgrading mariculture and also sponsored by K.C.Wong Magna Fund in Ningbo University. We thank Nature Research Editing Service for English language editing.
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Communicated by Jorge Membrillo-Hernández.
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Zhang, D., He, S., Ming, T. et al. A metabonomic analysis on the response of Enterobacter cloacae from coastal outfall for land-based pollutant under phoxim stress. Arch Microbiol 199, 1165–1173 (2017). https://doi.org/10.1007/s00203-017-1383-0
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DOI: https://doi.org/10.1007/s00203-017-1383-0