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Updated: Mar 25, 2026

Population and Single-Cell Analysis of Antibiotic Persistence in Escherichia coli
Published on: March 24, 2023
DNA-crosslinker cisplatin eradicates bacterial persister cells
Nityananda Chowdhury1, Thammajun L Wood1, Mariano Martínez-Vázquez2
1Department of Chemical Engineering, Pennsylvania State University, University Park, 16802-4400, Pennsylvania.
Abstract:
For all bacteria, nearly every antimicrobial fails since a subpopulation of the bacteria enter a dormant state known as persistence, in which the antimicrobials are rendered ineffective due to the lack of metabolism. This tolerance to antibiotics makes microbial infections the leading cause of death worldwide and makes treating chronic infections, including those of wounds problematic. Here, we show that the FDA-approved anti-cancer drug cisplatin [cis-diamminodichloroplatinum(II)], which mainly forms intra-strand DNA crosslinks, eradicates Escherichia coli K-12 persister cells through a growth-independent mechanism. Additionally, cisplatin is more effective at killing Pseudomonas aeruginosa persister cells than mitomycin C, which forms inter-strand DNA crosslinks, and cisplatin eradicates the persister cells of several pathogens including enterohemorrhagic E. coli, Staphylococcus aureus, and P. aeruginosa. Cisplatin was also highly effective against clinical isolates of S. aureus and P. aeruginosa. Therefore, cisplatin has broad spectrum activity against persister cells. Biotechnol. Bioeng. 2016;113: 1984-1992. © 2016 Wiley Periodicals, Inc.
Insights
The anti-cancer drug cisplatin eradicates dormant bacterial persister cells, which are tolerant to antibiotics. This drug shows broad-spectrum activity against various pathogens, offering new hope for treating persistent infections.
Area of Science:
- Microbiology
- Drug Discovery
- Molecular Biology
Background:
- Bacterial persister cells survive antibiotic treatment by entering a dormant, non-metabolizing state.
- This antibiotic tolerance contributes to chronic infections and high mortality rates globally.
- Current antimicrobials are ineffective against these persister cells.
Purpose of the Study:
- To investigate the efficacy of the anti-cancer drug cisplatin against bacterial persister cells.
- To determine the mechanism of action of cisplatin on persister cells.
- To evaluate the broad-spectrum activity of cisplatin against various pathogenic bacteria.
Main Methods:
- Treatment of Escherichia coli K-12 persister cells with cisplatin.
- Comparison of cisplatin's efficacy with mitomycin C against Pseudomonas aeruginosa persister cells.
- Testing cisplatin against persister cells of clinical isolates of Staphylococcus aureus and P. aeruginosa.
Main Results:
- Cisplatin eradicated Escherichia coli K-12 persister cells via a growth-independent mechanism.
- Cisplatin was more effective than mitomycin C in killing Pseudomonas aeruginosa persister cells.
- Cisplatin demonstrated high efficacy against persister cells of multiple pathogens, including clinical isolates.
Conclusions:
- Cisplatin exhibits broad-spectrum activity against bacterial persister cells.
- Cisplatin represents a potential therapeutic agent for combating persistent bacterial infections.
- The anti-cancer drug cisplatin offers a novel strategy against antibiotic-tolerant bacteria.
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