Activated ADI pathway: the initiator of intermediate vancomycin resistance in Staphylococcus aureus

Tan XE 1 , Neoh HM 1 , Looi ML 1 , Chin SF 1 , Cui L 2 , Hiramatsu K 3 Show all authors , Hussin S 4 , Jamal R 1

Affiliations 

  • 1 a UKM Medical Molecular Biology Institute (UMBI), Universiti Kebangsaan Malaysia, Malaysia
  • 2 d Division of Bacteriology, Department of Infection and Immunity, School of Medicine, Jichi Medical University, Japan
  • 3 b Department of Bacteriology, School of Medicine, Juntendo University, Japan
  • 4 e Department of Medical Microbiology and Immunology, Universiti Kebangsaan Malaysia, Malaysia
Can J Microbiol, 2017 Mar;63(3):260-264.
PMID: 28059579 DOI: 10.1139/cjm-2016-0439

Abstract

Comparative proteomic profiling between 2 vancomycin-intermediate Staphylococcus aureus (VISA) strains, Mu50Ω-vraSm and Mu50Ω-vraSm-graRm, and vancomycin-susceptible S. aureus (VSSA) strain Mu50Ω revealed upregulated levels of catabolic ornithine carbamoyltransferase (ArcB) of the arginine catabolism pathway in VISA strains. Subsequent analyses showed that the VISA strains have higher levels of cellular ATP and ammonia, which are by-products of arginine catabolism, and displayed thicker cell walls. We postulate that elevated cytoplasmic ammonia and ATP molecules, resulting from activated arginine catabolism upon acquisition of vraS and graR mutations, are important requirements facilitating cell wall biosynthesis, thereby contributing to thickened cell wall and consequently reduced vancomycin susceptibility in VISA strains.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.

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