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Cefoperazone-treated Mouse Model of Clinically-relevant Clostridium difficile Strain R20291
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Enterococci enhance Clostridioides difficile pathogenesis.

Alexander B Smith1, Matthew L Jenior2, Orlaith Keenan1

  • 1Division of Protective Immunity, Children's Hospital of Philadelphia, Philadelphia, PA, USA.

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|November 17, 2022
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Summary
This summary is machine-generated.

Opportunistic gut bacteria, enterococci, boost Clostridioides difficile virulence by altering the gut metabolic environment. This interaction, involving nutrient exchange and metabolic reprogramming, increases C. difficile fitness and pathogenesis.

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Area of Science:

  • Microbiology
  • Gut Microbiome Research
  • Infectious Diseases

Background:

  • The gastrointestinal tract harbors a complex polymicrobial community influencing host health and disease.
  • Microbial interactions are crucial in infections, yet mechanisms by which commensal or pathogenic microbiota affect pathogen virulence are not fully understood.
  • Clostridioides difficile infection (CDI) is a major healthcare concern, often exacerbated by disruptions in the gut microbiota.

Purpose of the Study:

  • To investigate how the expansion of enterococci, a group of antibiotic-resistant opportunistic pathogens, impacts the fitness and pathogenesis of Clostridioides difficile.
  • To elucidate the metabolic mechanisms underlying the interaction between enterococci and C. difficile in the gut environment.
  • To provide mechanistic insights into the role of pathogenic microbiota in CDI severity.

Main Methods:

  • Utilized mouse models of infection to study microbial interactions in vivo.
  • Analyzed metabolic changes in the gut environment shaped by enterococci.
  • Investigated the reprogramming of C. difficile metabolism in response to enterococcal-derived nutrients and metabolic cues.
  • Examined patient samples from individuals with C. difficile infection.

Main Results:

  • Expansion of enterococci enhances the fitness and pathogenesis of Clostridioides difficile in the gut.
  • Enterococci reshape the gut metabolic landscape through nutrient restriction and cross-feeding, providing fermentable amino acids (leucine, ornithine) that benefit C. difficile.
  • Enterococcal depletion of arginine acts as a metabolic cue, increasing C. difficile virulence.
  • Microbial interactions between enterococci and C. difficile were observed in mouse models and human CDI patients.

Conclusions:

  • Enterococci promote C. difficile pathogenesis by modulating the gut metabolic environment.
  • Specific metabolic exchanges, including nutrient provision and depletion, mediate the enhanced virulence of C. difficile in the presence of enterococci.
  • These findings highlight the significant role of pathogenic microbiota in driving the severity of C. difficile infections.