Mechanisms of stress-activated persister formation in Escherichia coli

Stephanie M. Amato, Mark P. Brynildsen

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Within bacterial populations, small subpopulations of cells have the capacity to survive supralethal concentrations of antibiotics without the aid of genetically acquired resistance. Since these persister cells have been linked to antibiotic treatment failure in chronic and recurring infections, understanding the pathways that transform normal cells into persisters will aid in the discovery of more effective treatments for recalcitrant infections. Recent work has found that numerous stresses, including antibiotic treatment, starvation, and metabolic transitions, initiate cascades that result in persister formation. Here, these phenomena are discussed in the context of the signaling pathways that transduce stress responses through cellular networks to yield antibiotic tolerance. Overall, these mechanisms can be quite distinct, but some mediators, such as ppGpp, are critical to multiple pathways and, therefore, are promising targets for the development of therapies for the treatment of recurring infections.

Original languageEnglish (US)
Title of host publicationStress and Environmental Regulation of Gene Expression and Adaptation in Bacteria
PublisherWiley-Blackwell
Pages446-453
Number of pages8
Volume1
ISBN (Electronic)9781119004813
ISBN (Print)9781119004882
DOIs
StatePublished - Aug 12 2016

All Science Journal Classification (ASJC) codes

  • Immunology and Microbiology(all)

Keywords

  • Antibiotic tolerance
  • Bacterial persistence
  • PpGpp
  • Stress response
  • Toxin-antitoxin systems

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