The Intraperitoneal Transcriptome of the Opportunistic Pathogen Enterococcus faecalis in Mice

Cécile Muller1, Margherita Cacaci2, Nicolas Sauvageot1

  • 1U2RM-Stress and Virulence, University of Caen Basse-Normandie, EA4655, 14032 Caen, France.

Plos One
|May 16, 2015
PubMed

Insights

Enterococcus faecalis adapts to host conditions by altering gene expression, inducing virulence factors and metabolic pathways like glycerol catabolism. Impaired glycerol metabolism significantly reduces bacterial organ colonization during infection.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Infectious Diseases

Background:

  • Enterococcus faecalis is an opportunistic pathogen with significant virulence potential.
  • Understanding bacterial adaptation to host environments is crucial for combating infections.

Purpose of the Study:

  • To investigate the in vivo gene expression profile of Enterococcus faecalis during infection.
  • To identify key adaptive mechanisms and virulence factors utilized by the bacterium within a host.

Main Methods:

  • Transcriptome analysis using RNA-sequencing of E. faecalis isolated from a mouse peritonitis model.
  • Identification of differentially expressed genes (induced and repressed).
  • Validation of gene function through virulence assays using mutant strains.

Main Results:

  • RNA-sequencing revealed 211 induced and 157 repressed genes in vivo.
  • Induced genes included major virulence factors (cytolysin, gelatinase) and stress response proteins.
  • Metabolic genes, particularly those for glycerol and α-/β-glucoside utilization, were significantly upregulated, suggesting adaptation to host nutrients.
  • Mutants deficient in glycerol metabolism showed reduced organ colonization in a mouse model.

Conclusions:

  • Enterococcus faecalis actively modifies its gene expression to survive and thrive in host conditions.
  • Glycerol metabolism is a critical factor for E. faecalis virulence and colonization.
  • The pentose phosphate pathway may be favored over glycolysis for increased reducing power production during infection.

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