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In vitro resistance of Staphylococcus aureus to thrombin-induced platelet microbicidal protein is associated with

A S Bayer1, R Prasad, J Chandra

  • 1Research and Education Institute, St. John's Cardiovascular Research Center and the Division of Infectious Diseases, Harbor-UCLA Medical Center, Torrance, California, 90509, USA. Bayer@humc.edu

Infection and Immunity
|May 19, 2000
PubMed

Insights

Staphylococcus aureus strains resistant to platelet microbicidal proteins (PMPs) have altered cell membranes. These resistant strains show increased membrane fluidity due to higher levels of specific lipids, impacting PMP effectiveness.

Area of Science:

  • Microbiology
  • Biochemistry
  • Infectious Diseases

Background:

  • Platelet microbicidal proteins (PMPs) are crucial for combating bloodstream infections like Staphylococcus aureus.
  • Previous studies linked resistance to thrombin-induced PMP-1 (tPMP-1) in S. aureus with increased endocarditis severity.
  • The precise mechanisms behind tPMP-1 resistance in S. aureus remain incompletely understood.

Purpose of the Study:

  • To investigate the underlying mechanisms of tPMP-1 resistance in Staphylococcus aureus.
  • To compare membrane structure and function in tPMP-1-resistant and susceptible S. aureus strains.
  • To elucidate how alterations in the bacterial cell membrane contribute to PMP resistance.

Main Methods:

  • Generated tPMP-1 resistant (tPMP-1(r)) S. aureus strains via transposon mutagenesis, serial passage, or plasmid carriage (pSK1).
  • Analyzed and compared membrane lipid composition, focusing on chain length and unsaturation.
  • Assessed cell membrane fluidity using fluorescence polarization in paired resistant and susceptible strains.

Main Results:

  • All tPMP-1(r) strains exhibited elevated levels of longer-chain, unsaturated membrane lipids compared to their tPMP-1 susceptible (tPMP-1(s)) counterparts.
  • A significant increase in cell membrane fluidity was observed in tPMP-1(r) strains.
  • Fluorescence polarization measurements confirmed higher membrane fluidity in resistant strains.

Conclusions:

  • Specific alterations in the cytoplasmic membrane composition are associated with tPMP-1 resistance in S. aureus.
  • Increased membrane fluidity, driven by changes in lipid profiles, is a key factor in S. aureus resistance to tPMP-1.
  • These findings deepen our understanding of antimicrobial resistance mechanisms in bacterial pathogens.

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