Exogenous D-ribose promotes gentamicin treatment of several drug-resistant Salmonella

Bibliographic Details
Title: Exogenous D-ribose promotes gentamicin treatment of several drug-resistant Salmonella
Authors: Yanhong Zhou, Yan Yong, Chunyang Zhu, Heng Yang, Binghu Fang
Source: Frontiers in Microbiology, Vol 13 (2022)
Publisher Information: Frontiers Media S.A., 2022.
Publication Year: 2022
Collection: LCC:Microbiology
Subject Terms: D-ribose, gentamicin, Salmonella, metabolomics, resistance, Microbiology, QR1-502
More Details: The metabolic microenvironment of bacteria impacts drug efficacy. However, the metabolic mechanisms of drug-resistant Salmonella spp. remain largely unknown. This study characterized the metabolic mechanism of gentamicin-resistant Salmonella Choleraesuis and found that D-ribose increased the gentamicin-mediated killing of this bacteria. Non-targeted metabolomics of homologous gentamicin-susceptible Salmonella Choleraesuis (SCH-S) and gentamicin-resistant S. Choleraesuis (SCH-R) was performed using UHPLC-Q-TOF MS. The metabolic signature of SCH-R included disrupted central carbon metabolism and energy metabolism, along with dysregulated amino acid and nucleotide metabolism, vitamin and cofactor metabolism, and fatty acid synthesis. D-ribose, the most suppressed metabolite in SCH-R, was shown to strengthen gentamicin efficacy against SCH-R and a clinically isolated multidrug-resistant strain. This metabolite had a similar impact on Salmonella. Derby and Salmonella. Typhimurium. D-ribose activates central carbon metabolism including glycolysis, the pentose phosphate pathway (PPP), and the tricarboxylic acid cycle (TCA cycle), increases the abundance of NADH, polarizes the electron transport chain (ETC), and elevates the proton motive force (PMF) of cells, and induces drug uptake and cell death. These findings suggest that central carbon metabolism plays a critical role in the acquisition of gentamicin resistance by Salmonella, and that D-ribose may serve as an antibiotic adjuvant for gentamicin treatment of resistant bacterial infections.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 1664-302X
Relation: https://www.frontiersin.org/articles/10.3389/fmicb.2022.1053330/full; https://doaj.org/toc/1664-302X
DOI: 10.3389/fmicb.2022.1053330
Access URL: https://doaj.org/article/26fa8ecf675f457db2c830b54fec9698
Accession Number: edsdoj.26fa8ecf675f457db2c830b54fec9698
Database: Directory of Open Access Journals
More Details
ISSN:1664302X
DOI:10.3389/fmicb.2022.1053330
Published in:Frontiers in Microbiology
Language:English