Antibacterial Peptides Resistance in Staphylococcus aureus: Various Mechanisms and the Association with Pathogenicity

Miki Kawada-Matsuo1, Mi Nguyen-Tra Le1, Hitoshi Komatsuzawa1

  • 1Department of Bacteriology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima 734-8551, Japan.

Genes
|October 23, 2021
PubMed

Insights

Highly nisin A-resistant Staphylococcus aureus mutants were developed using specific mutations in two-component systems (TCSs) and PmtR. Some resistant strains exhibited increased pathogenicity, highlighting a link between resistance and virulence.

Area of Science:

  • Microbiology and Molecular Biology
  • Bacterial Pathogenesis
  • Antimicrobial Resistance

Background:

  • Staphylococcus aureus colonizes human hosts by resisting antibacterial factors, including bacteriocins.
  • Two-component systems (TCSs) in S. aureus confer resistance to bacteriocins, but only at low concentrations.
  • Nisin A, a bacteriocin used as a food preservative, is produced by Lactococcus lactis.

Purpose of the Study:

  • To isolate highly nisin A-resistant Staphylococcus aureus mutants.
  • To investigate the genetic basis of high-level bacteriocin resistance.
  • To explore the association between antimicrobial peptide resistance and bacterial pathogenicity.

Main Methods:

  • Exposure of S. aureus to sub-inhibitory concentrations of nisin A to select for resistant mutants.
  • Identification of mutations in identified resistant strains.
  • Assessment of pathogenicity in highly resistant S. aureus isolates.

Main Results:

  • Isolation of highly nisin A-resistant S. aureus mutants.
  • Identification of mutations in the BraRS two-component system (TCS) and PmtR regulator in resistant strains.
  • Observation of increased pathogenicity in some highly nisin A-resistant S. aureus strains.

Conclusions:

  • The BraRS TCS and PmtR play crucial roles in conferring high-level resistance to nisin A in S. aureus.
  • High-level antimicrobial peptide resistance in S. aureus can be associated with enhanced pathogenicity.
  • Findings provide insights into TCS-mediated resistance mechanisms and their link to virulence in S. aureus.

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