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Characterization of Toxin-Antitoxin (TA) Systems in Pseudomonas aeruginosa Clinical Isolates in Iran

Mohammad Savari1, Soodabeh Rostami2, Alireza Ekrami3

  • 1Department of Microbiology, Medicine school, Tehran University of Medical Sciences, Tehran, IR Iran.

Jundishapur Journal of Microbiology
|April 22, 2016
PubMed
Abstract

Insights

Toxin-antitoxin systems, including relBE and higBA, are widespread in Pseudomonas aeruginosa clinical isolates. Their prevalence suggests these bacterial systems could be novel antimicrobial therapy targets.

Area of Science:

  • Microbiology
  • Bacterial genetics

Background:

  • Pseudomonas aeruginosa is a significant pathogen in both hospital and community settings.
  • Toxin-antitoxin (TA) systems are bacterial regulatory elements with potential as antimicrobial targets.
  • The prevalence of TA systems in clinical P. aeruginosa isolates is largely unknown.

Purpose of the Study:

  • To characterize the prevalence and genetic location of three TA systems (parDE, relBE, higBA) in P. aeruginosa clinical isolates.
  • To investigate the distribution of these TA systems within clinical P. aeruginosa strains.

Main Methods:

  • Typing of clinical isolates using ERIC-PCR and BOX-PCR.
  • Detection of parDE, relBE, and higBA genes in 174 P. aeruginosa isolates.
  • Analysis of flanking regions to determine chromosomal or plasmid location of TA systems.

Main Results:

  • The relBE and higBA systems were found in all P. aeruginosa isolates, while parDE was less common.
  • Flanking regions were amplified for parDE in all positive isolates, and for nearly all relBE genes.
  • The higBA locus showed amplification of downstream sequences in all strains and upstream sequences in most strains.

Conclusions:

  • Toxin-antitoxin systems are highly prevalent in P. aeruginosa clinical isolates.
  • The widespread presence of these TA systems indicates their potential as novel targets for antimicrobial drug development.
Keywords:
Gene Regulatory NetworksGenotypingPseudomonas aeruginosaResistance

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