The mechanisms that regulate Vibrio parahaemolyticus virulence gene expression differ between pathotypes

Nicholas Petronella1, Jennifer Ronholm2,3

  • 11​Biostatistics and Modelling Division, Bureau of Food Surveillance and Science Integration, Food Directorate, Health Canada, Ottawa, ON, Canada.

Microbial Genomics
|May 30, 2018
PubMed

Insights

Most Vibrio parahaemolyticus are non-pathogenic, but some acquire genomic pathogenicity islands (PAIs). This study reveals bile does not up-regulate virulence genes in canonical strains, suggesting new virulence factors in non-canonical strains warrant investigation.

Area of Science:

  • Microbiology
  • Genomics
  • Bacterial Pathogenesis

Background:

  • Most Vibrio parahaemolyticus from marine environments are non-pathogenic.
  • Pathogenic strains possess genomic pathogenicity islands (PAIs) encoding toxins like TDH/TRH and T3SS2.
  • Non-canonical V. parahaemolyticus isolates lacking PAIs have been found in clinical settings, prompting research into novel virulence factors.

Purpose of the Study:

  • To investigate differential gene expression in V. parahaemolyticus isolates with varying pathogenic profiles upon exposure to crude bile.
  • To determine if bile acts as a virulence gene expression signal in different V. parahaemolyticus pathotypes.
  • To identify potential novel virulence factors in non-canonical V. parahaemolyticus isolates.

Main Methods:

  • Comparative analysis of gene expression in four V. parahaemolyticus isolates: one canonical pathogenic strain (TDH, TRH, T3SS2 positive) and three non-canonical strains (two clinical, one environmental) lacking PAIs.
  • Exposure of isolates to crude bile to assess its effect on virulence gene expression.
  • Differential gene expression analysis to identify up-regulated genes in response to bile.

Main Results:

  • Virulence gene expression was not up-regulated by crude bile in the canonical TDH-positive, TRH-positive V. parahaemolyticus strain.
  • This finding challenges the established understanding of bile as a universal virulence signal in V. parahaemolyticus.
  • Several genes of interest were identified as up-regulated in the non-canonical V. parahaemolyticus pathotypes exposed to bile, suggesting potential novel virulence mechanisms.

Conclusions:

  • The regulation of virulence genes by bile in V. parahaemolyticus is pathotype-specific and requires further investigation.
  • The current dogma regarding bile-induced virulence gene expression in V. parahaemolyticus needs revision.
  • The identified up-regulated genes in non-canonical isolates represent promising candidates for novel virulence factors contributing to V. parahaemolyticus pathogenesis.

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