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Bacterial signaling can occur within bacteria (intracellular) or between bacteria (intercellular). At times, a group of bacteria behaves like a community. To achieve this, they engage in quorum sensing, the perception of higher cell density that causes changes in gene expression. Quorum sensing involves both extracellular and intracellular signaling. The signaling cascade starts with a molecule called an autoinducer (AI). Individual bacteria produce AIs that move out of the bacterial cell...
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Related Experiment Video

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A Rapid Image-based Bacterial Virulence Assay Using Amoeba
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Dismantling the bacterial virulence program.

Morgan A Alford1, Daniel Pletzer1, Robert E W Hancock1

  • 1Centre for Microbial Diseases and Immunity Research, Department of Microbiology and Immunology, University of British Columbia, Vancouver, BC, Canada.

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|March 14, 2019
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Summary
This summary is machine-generated.

Targeting bacterial adaptive resistance, a reversible non-mutational survival mechanism, is crucial for developing new anti-infective compounds. Interfering with stress-response proteins can dismantle bacterial virulence and combat rising antimicrobial resistance.

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Area of Science:

  • Microbiology
  • Infectious Diseases
  • Drug Discovery

Background:

  • Rising antimicrobial resistance necessitates novel anti-infective strategies.
  • Adaptive resistance, a reversible bacterial phenotype, allows survival against antibiotics without mutation.
  • This resistance is triggered by in vivo stressors and is clinically prevalent, often linked to biofilm formation.

Purpose of the Study:

  • To highlight the importance of targeting stress-response effectors.
  • To explore the potential of these targets in combating adaptive resistance and virulence.
  • To propose a strategy for developing new anti-infective therapies.

Main Methods:

  • The study focuses on the conceptual framework of targeting adaptive resistance mechanisms.
  • It emphasizes the role of stress-response proteins in bacterial survival and virulence.
  • The approach involves understanding in vivo bacterial adaptation.

Main Results:

  • Adaptive resistance is a significant challenge in treating bacterial infections.
  • Stress-response pathways are key contributors to bacterial virulence and survival in vivo.
  • Targeting these pathways offers a promising strategy to enhance antibiotic efficacy.

Conclusions:

  • Interfering with stress-response proteins can dismantle bacterial virulence.
  • This approach provides a means to treat infectious diseases, especially in combination with conventional antibiotics.
  • Developing anti-infective compounds that target adaptive resistance is essential for future therapeutic success.