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

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 gentami...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Yanhong Zhou [verfasserIn] Yan Yong [verfasserIn] Chunyang Zhu [verfasserIn] Heng Yang [verfasserIn] Binghu Fang [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	D-ribose gentamicin Salmonella metabolomics resistance

Übergeordnetes Werk:	In: Frontiers in Microbiology - Frontiers Media S.A., 2011, 13(2022)
Übergeordnetes Werk:	volume:13 ; year:2022

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fmicb.2022.1053330

Katalog-ID:	DOAJ08359048X

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spelling	10.3389/fmicb.2022.1053330 doi (DE-627)DOAJ08359048X (DE-599)DOAJ26fa8ecf675f457db2c830b54fec9698 DE-627 ger DE-627 rakwb eng QR1-502 Yanhong Zhou verfasserin aut Exogenous D-ribose promotes gentamicin treatment of several drug-resistant Salmonella 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. D-ribose gentamicin Salmonella metabolomics resistance Microbiology Yanhong Zhou verfasserin aut Yan Yong verfasserin aut Chunyang Zhu verfasserin aut Chunyang Zhu verfasserin aut Heng Yang verfasserin aut Heng Yang verfasserin aut Binghu Fang verfasserin aut Binghu Fang verfasserin aut In Frontiers in Microbiology Frontiers Media S.A., 2011 13(2022) (DE-627)642889384 (DE-600)2587354-4 1664302X nnns volume:13 year:2022 https://doi.org/10.3389/fmicb.2022.1053330 kostenfrei https://doaj.org/article/26fa8ecf675f457db2c830b54fec9698 kostenfrei https://www.frontiersin.org/articles/10.3389/fmicb.2022.1053330/full kostenfrei https://doaj.org/toc/1664-302X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2022
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allfieldsGer	10.3389/fmicb.2022.1053330 doi (DE-627)DOAJ08359048X (DE-599)DOAJ26fa8ecf675f457db2c830b54fec9698 DE-627 ger DE-627 rakwb eng QR1-502 Yanhong Zhou verfasserin aut Exogenous D-ribose promotes gentamicin treatment of several drug-resistant Salmonella 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. D-ribose gentamicin Salmonella metabolomics resistance Microbiology Yanhong Zhou verfasserin aut Yan Yong verfasserin aut Chunyang Zhu verfasserin aut Chunyang Zhu verfasserin aut Heng Yang verfasserin aut Heng Yang verfasserin aut Binghu Fang verfasserin aut Binghu Fang verfasserin aut In Frontiers in Microbiology Frontiers Media S.A., 2011 13(2022) (DE-627)642889384 (DE-600)2587354-4 1664302X nnns volume:13 year:2022 https://doi.org/10.3389/fmicb.2022.1053330 kostenfrei https://doaj.org/article/26fa8ecf675f457db2c830b54fec9698 kostenfrei https://www.frontiersin.org/articles/10.3389/fmicb.2022.1053330/full kostenfrei https://doaj.org/toc/1664-302X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2022
allfieldsSound	10.3389/fmicb.2022.1053330 doi (DE-627)DOAJ08359048X (DE-599)DOAJ26fa8ecf675f457db2c830b54fec9698 DE-627 ger DE-627 rakwb eng QR1-502 Yanhong Zhou verfasserin aut Exogenous D-ribose promotes gentamicin treatment of several drug-resistant Salmonella 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. D-ribose gentamicin Salmonella metabolomics resistance Microbiology Yanhong Zhou verfasserin aut Yan Yong verfasserin aut Chunyang Zhu verfasserin aut Chunyang Zhu verfasserin aut Heng Yang verfasserin aut Heng Yang verfasserin aut Binghu Fang verfasserin aut Binghu Fang verfasserin aut In Frontiers in Microbiology Frontiers Media S.A., 2011 13(2022) (DE-627)642889384 (DE-600)2587354-4 1664302X nnns volume:13 year:2022 https://doi.org/10.3389/fmicb.2022.1053330 kostenfrei https://doaj.org/article/26fa8ecf675f457db2c830b54fec9698 kostenfrei https://www.frontiersin.org/articles/10.3389/fmicb.2022.1053330/full kostenfrei https://doaj.org/toc/1664-302X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2022
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source	In Frontiers in Microbiology 13(2022) volume:13 year:2022
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authorswithroles_txt_mv	Yanhong Zhou @@aut@@ Yan Yong @@aut@@ Chunyang Zhu @@aut@@ Heng Yang @@aut@@ Binghu Fang @@aut@@
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callnumber-first	Q - Science
author	Yanhong Zhou
spellingShingle	Yanhong Zhou misc QR1-502 misc D-ribose misc gentamicin misc Salmonella misc metabolomics misc resistance misc Microbiology Exogenous D-ribose promotes gentamicin treatment of several drug-resistant Salmonella
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topic_title	QR1-502 Exogenous D-ribose promotes gentamicin treatment of several drug-resistant Salmonella D-ribose gentamicin Salmonella metabolomics resistance
topic	misc QR1-502 misc D-ribose misc gentamicin misc Salmonella misc metabolomics misc resistance misc Microbiology
topic_unstemmed	misc QR1-502 misc D-ribose misc gentamicin misc Salmonella misc metabolomics misc resistance misc Microbiology
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title	Exogenous D-ribose promotes gentamicin treatment of several drug-resistant Salmonella
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title_full	Exogenous D-ribose promotes gentamicin treatment of several drug-resistant Salmonella
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title_sort	exogenous d-ribose promotes gentamicin treatment of several drug-resistant salmonella
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title_auth	Exogenous D-ribose promotes gentamicin treatment of several drug-resistant Salmonella
abstract	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.
abstractGer	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.
abstract_unstemmed	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.
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title_short	Exogenous D-ribose promotes gentamicin treatment of several drug-resistant Salmonella
url	https://doi.org/10.3389/fmicb.2022.1053330 https://doaj.org/article/26fa8ecf675f457db2c830b54fec9698 https://www.frontiersin.org/articles/10.3389/fmicb.2022.1053330/full https://doaj.org/toc/1664-302X
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author2	Yanhong Zhou Yan Yong Chunyang Zhu Heng Yang Binghu Fang
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up_date	2024-07-03T18:19:33.281Z
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Exogenous D-ribose promotes gentamicin treatment of several drug-resistant Salmonella

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