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Metabolite-enabled eradication of bacterial persisters by aminoglycosides

Author

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  • Kyle R. Allison

    (Howard Hughes Medical Institute, Center for Biodynamics and Center for Advanced Biotechnology, Boston University)

  • Mark P. Brynildsen

    (Howard Hughes Medical Institute, Center for Biodynamics and Center for Advanced Biotechnology, Boston University
    Present address: Department of Chemical and Biological Engineering, Princeton University, Princeton, New Jersey 08544, USA.)

  • James J. Collins

    (Howard Hughes Medical Institute, Center for Biodynamics and Center for Advanced Biotechnology, Boston University
    Boston University School of Medicine, 715 Albany Street
    Wyss Institute for Biologically Inspired Engineering, Harvard University)

Abstract

How metabolic 'helpers' kill persistent pathogens Bacterial cells can enter a dormant 'persister' state that leaves them more resistant to stress conditions, including killing by antibiotics. In a clinical setting, persister formation can lead to incomplete eradication of bacterial pathogens and treatment failure. James Collins and colleagues show that certain metabolic stimuli (including glucose and pyruvate) can increase killing of persister cells by aminoglycoside antibiotics including gentamicin. This raises the prospect that the delivery of metabolites as adjuvants to aminoglycosides could be effective in the treatment of chronic bacterial infections.

Suggested Citation

  • Kyle R. Allison & Mark P. Brynildsen & James J. Collins, 2011. "Metabolite-enabled eradication of bacterial persisters by aminoglycosides," Nature, Nature, vol. 473(7346), pages 216-220, May.
    • Handle: RePEc:nat:nature:v:473:y:2011:i:7346:d:10.1038_nature10069
    DOI: 10.1038/nature10069
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    Cited by:

    1. Weijun Xiu & Ling Wan & Kaili Yang & Xiao Li & Lihui Yuwen & Heng Dong & Yongbin Mou & Dongliang Yang & Lianhui Wang, 2022. "Potentiating hypoxic microenvironment for antibiotic activation by photodynamic therapy to combat bacterial biofilm infections," Nature Communications, Nature, vol. 13(1), pages 1-13, December.

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