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Related Experiment Video

Updated: Nov 22, 2025

LED-Based In Vitro Screening for Assessing Photoactivable Molecules in Bacterial Photodynamic Inactivation
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Staphylococcus aureus Tolerance and Genomic Response to Photodynamic Inactivation.

Sara B Snell1, Ann Lindley Gill1, Constantine G Haidaris1,2

  • 1Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, New York, USA.

Msphere
|January 7, 2021
PubMed
Summary

Photodynamic inactivation (PDI) offers a promising alternative to antibiotics for treating Staphylococcus aureus infections. Repeated PDI exposure can lead to bacterial resistance, primarily through mutations in the QsrR gene, which regulates the cell's response to PDI.

Keywords:
PDI tolerancePDI transcriptomegenomic adaptationphotodynamic inactivationtolerance

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Area of Science:

  • Microbiology
  • Antimicrobial Resistance
  • Photodynamic Therapy

Background:

  • Staphylococcus aureus is a significant pathogen causing infections ranging from skin colonization to invasive disease.
  • Antibiotic resistance in S. aureus leads to treatment failures and increased mortality.
  • Photodynamic inactivation (PDI) is an emerging alternative to conventional antibiotics.

Purpose of the Study:

  • To investigate the mechanisms of S. aureus tolerance and resistance to PDI.
  • To identify global cellular responses and genetic adaptations to PDI exposure.
  • To elucidate the role of specific genes and mutations in PDI tolerance.

Main Methods:

  • Exposure of S. aureus strains (HG003 and isogenic mutants) to single or multiple PDI doses.
  • Assessment of bacterial survival and tolerance.
  • Global transcriptome and genome analyses to identify adaptive mutations and regulatory changes.

Main Results:

  • PDI exposure induced tolerance associated with superoxide dismutase and the methylhydroquinone (MHQ)-quinone transcriptome network.
  • Genome analysis revealed a key mutation in the QsrR transcriptional repressor in PDI-tolerant strains.
  • Repeated PDI treatment led to the acquisition of heritable QsrR mutations, demonstrating adaptive resistance.
  • Deletion of the qsrR gene confirmed its regulatory role in S. aureus response to PDI.

Conclusions:

  • S. aureus can develop tolerance and resistance to PDI through specific genetic adaptations.
  • The QsrR repressor plays a critical role in mediating the bacterial response to PDI.
  • Understanding these resistance mechanisms is crucial for refining PDI as an adjunctive therapy for S. aureus infections.