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Articles linked to this work by shared authors, journal, and citation graph.

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Mechanistic insights into the pathogenesis and therapeutic recalcitrance of <i>Staphylococcus aureus</i> osteomyelitis.

Clinical microbiology reviews·2026
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<i>Staphylococcus aureus</i> Proteins Implicated in the Reduced Virulence of <i>sarA</i> and <i>sarA/agr</i> Mutants in Osteomyelitis.

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The ability of <i>sarA</i> to limit protease production plays a key role in the pathogenesis of <i>Staphylococcus aureus</i> osteomyelitis irrespective of the functional status of <i>agr</i>.

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Increased production of aureolysin and staphopain A is a primary determinant of the reduced virulence of <i>Staphylococcus aureus sarA</i> mutants in osteomyelitis.

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Comparative evaluation of small molecules reported to be inhibitors of <i>Staphylococcus aureus</i> biofilm formation.

Microbiology spectrum·2023
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The major role of <i>sarA</i> in limiting <i>Staphylococcus aureus</i> extracellular protease production <i>in vitro</i> is correlated with decreased virulence in diverse clinical isolates in osteomyelitis.

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Updated: May 5, 2026

Targeting Biofilm Associated Staphylococcus aureus Using Resazurin Based Drug-susceptibility Assay
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Staphylococcus aureus Biofilm-Associated Infections: Have We Found a Clinically Relevant Target?

Karen E Beenken1,2, Mark S Smeltzer1,3

  • 1Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.

Microorganisms
|April 26, 2025
PubMed
Summary

Staphylococcus aureus biofilm formation poses a significant challenge due to intrinsic antibiotic resistance. This review assesses the validation of sarA as a therapeutic target to combat these persistent infections.

Keywords:
Staphylococcus aureusagrbiofilmosteomyelitisproteaseregulationsarAsigBxerC

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Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Drug Discovery

Background:

  • Staphylococcus aureus is a highly adaptable pathogen causing diverse infections.
  • Biofilm formation in S. aureus contributes to intrinsic antibiotic resistance, complicating treatment.
  • Developing anti-biofilm strategies is crucial for clinical efficacy.

Purpose of the Study:

  • To evaluate regulatory loci in S. aureus biofilm formation as potential therapeutic targets.
  • To assess the clinical viability of sarA as a validated anti-biofilm target.
  • To guide the development of novel anti-biofilm agents.

Main Methods:

  • Literature review of S. aureus biofilm formation mechanisms.
  • Analysis of studies screening for biofilm inhibitors.
  • Evaluation of target validation strategies for anti-biofilm drug development.

Main Results:

  • Many S. aureus infections involve biofilms, conferring intrinsic resistance.
  • Numerous compounds have been screened for biofilm inhibition, but few overcome intrinsic resistance.
  • Limited studies focus on validating specific biofilm targets for therapeutic development.

Conclusions:

  • Targeting S. aureus biofilm formation is clinically valuable.
  • SarA requires further rigorous validation to be considered a primary therapeutic target.
  • Developing effective anti-biofilm strategies necessitates validated targets and optimized inhibitors.