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Bio-energetics Investigation of Candida albicans Using Real-time Extracellular Flux Analysis
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Energy depletion protects Candida albicans against antimicrobial peptides by rigidifying its cell membrane

Enno C I Veerman1, Marianne Valentijn-Benz, Kamran Nazmi

  • 1Department of Oral Biochemistry, Academic Centre for Dentistry Amsterdam, Vrije Universiteit and Universiteit van Amsterdam, 1081 BT Amsterdam, The Netherlands. eci.veerman@vumc.nl

The Journal of Biological Chemistry
|May 9, 2007
PubMed

Insights

Inhibitors blocking yeast energy metabolism prevent killing by antimicrobial peptides like Histatin 5. This resistance stems from changes in the yeast cell membrane

Area of Science:

  • Microbiology
  • Biochemistry
  • Cell Biology

Background:

  • Cationic antimicrobial peptides (CAPs) are crucial for innate immunity.
  • Yeast cells exhibit resistance to certain CAPs when their energy metabolism is inhibited.
  • Histatin 5 is a salivary CAP effective against Candida albicans.

Purpose of the Study:

  • To investigate the molecular mechanisms behind yeast resistance to Histatin 5.
  • To determine the role of cell membrane properties in this resistance phenomenon.

Main Methods:

  • Utilized Candida albicans as a model system.
  • Employed confocal and electron microscopy to visualize peptide entry.
  • Manipulated cell membrane fluidity and rigidity using benzyl alcohol, low temperatures, and Me(2)SO.
  • Assessed yeast cell membrane potential and energy charge.

Main Results:

  • Sodium azide blocked Histatin 5 entry at the cell wall level without significant membrane depolarization.
  • Increased membrane fluidity restored sensitivity to Histatin 5 in energy-depleted cells.
  • Membrane rigidification enhanced resistance to Histatin 5, independent of cellular energy levels.
  • Azide treatment altered the physical state of the lipid bilayer.

Conclusions:

  • The physical state of the yeast cell membrane is a key determinant of resistance to Histatin 5.
  • Inhibiting energy metabolism confers resistance by altering membrane properties, not solely through membrane potential changes.
  • Targeting membrane physical properties could be a strategy to overcome antimicrobial peptide resistance.

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