Minocycline Inhibits Candida albicans Budded-to-Hyphal-Form Transition and Biofilm Formation

Jpn J Infect Dis. 2017 Sep 25;70(5):490-494. doi: 10.7883/yoken.JJID.2016.369. Epub 2017 Mar 28.

Abstract

Candida albicans frequently causes bloodstream infections; its budded-to-hyphalform transition (BHT) and biofilm formation are major contributors to virulence. During an analysis of antibacterial compounds that inhibit C. albicans BHT, we found that the tetracycline derivative minocycline inhibited BHT and subsequent biofilm formation. Minocycline decreased expression of hypha-specific genes HWP1 and ECE1, and adhesion factor gene ALS3 of C. albicans. In addition, minocycline decreased cell surface hydrophobicity and the extracellular β-glucan level in biofilms. Minocycline has been widely used for catheter antibiotic lock therapy to prevent bacterial infection; this compound may also be prophylactically effective against Candida infection.

Keywords: Candida albicans; biofilm; budded-to-hyphal-form transition (BHT); minocycline; β-1,3-glucan.

MeSH terms

  • Antifungal Agents / pharmacology*
  • Biofilms / drug effects*
  • Biofilms / growth & development*
  • Candida albicans / chemistry
  • Candida albicans / drug effects*
  • Candida albicans / genetics
  • Candida albicans / physiology*
  • Fungal Proteins / biosynthesis
  • Fungal Proteins / genetics
  • Gene Expression Profiling
  • Hydrophobic and Hydrophilic Interactions
  • Membrane Glycoproteins / biosynthesis
  • Membrane Glycoproteins / genetics
  • Minocycline / pharmacology*
  • Surface Properties
  • beta-Glucans / analysis

Substances

  • ALS3 protein, Candida albicans
  • Antifungal Agents
  • ECE1 protein, Candida albicans
  • Fungal Proteins
  • HWP1 protein, Candida albicans
  • Membrane Glycoproteins
  • beta-Glucans
  • Minocycline