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Issue 7, 2017
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“On demand” redox buffering by H2S contributes to antibiotic resistance revealed by a bacteria-specific H2S donor

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Abstract

Understanding the mechanisms of antimicrobial resistance (AMR) will help launch a counter-offensive against human pathogens that threaten our ability to effectively treat common infections. Herein, we report bis(4-nitrobenzyl)sulfanes, which are activated by a bacterial enzyme to produce hydrogen sulfide (H2S) gas. We found that H2S helps maintain redox homeostasis and protects bacteria against antibiotic-triggered oxidative stress “on demand”, through activation of alternate respiratory oxidases and cellular antioxidants. We discovered, a hitherto unknown role for this gas, that chemical inhibition of H2S biosynthesis reversed antibiotic resistance in multidrug-resistant (MDR) uropathogenic Escherichia coli strains of clinical origin, whereas exposure to the H2S donor restored drug tolerance. Together, our study provides a greater insight into the dynamic defence mechanisms of this gas, modes of antibiotic action as well as resistance while progressing towards new pharmacological targets to address AMR.

Graphical abstract: “On demand” redox buffering by H2S contributes to antibiotic resistance revealed by a bacteria-specific H2S donor

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Publication details

The article was received on 24 Feb 2017, accepted on 20 Apr 2017 and first published on 27 Apr 2017


Article type: Edge Article
DOI: 10.1039/C7SC00873B
Citation: Chem. Sci., 2017,8, 4967-4972
  • Open access: Creative Commons BY license
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    “On demand” redox buffering by H2S contributes to antibiotic resistance revealed by a bacteria-specific H2S donor

    P. Shukla, V. S. Khodade, M. SharathChandra, P. Chauhan, S. Mishra, S. Siddaramappa, B. E. Pradeep, A. Singh and H. Chakrapani, Chem. Sci., 2017, 8, 4967
    DOI: 10.1039/C7SC00873B

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