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Related Experiment Videos

Colonization resistance: The deconvolution of a complex trait.

Erin E Olsan1, Mariana X Byndloss1, Franziska Faber1

  • 1From the Department of Medical Microbiology and Immunology, School of Medicine, University of California at Davis, Davis, California 95616.

The Journal of Biological Chemistry
|April 9, 2017
PubMed
Summary

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Antibiotic use increases the risk of carbapenemase-producing Enterobacteriaceae (CPE) gut colonization. Host cell metabolism, specifically respiratory electron acceptors, drives CPE expansion after antibiotics, offering potential intervention targets.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Gastroenterology

Background:

  • Carbapenemase-producing Enterobacteriaceae (CPE) pose a significant global hospital-acquired infection threat.
  • Antibiotic exposure is a known risk factor for developing CPE fecal carriage, potentially leading to nosocomial infections.

Purpose of the Study:

  • To review how antibiotics compromise colonization resistance against Enterobacteriaceae.
  • To identify potential control points for curbing the spread of CPE.

Main Methods:

  • Literature review focusing on the mechanisms by which antibiotics affect Enterobacteriaceae colonization.
  • Analysis of recent research identifying host-derived resources influencing bacterial expansion post-antibiotic treatment.

Main Results:

Keywords:
Escherichia coli (E. coli)Klebsiella pneumoniaSalmonella entericaantibiotic resistanceantibioticsmicrobiome

Related Experiment Videos

  • Antibiotics reduce the gut's natural resistance to Enterobacteriaceae colonization.
  • Host-derived respiratory electron acceptors are identified as a key resource enabling post-antibiotic Enterobacteriaceae expansion in the large bowel.

Conclusions:

  • Understanding the mechanistic insights into colonization resistance against Enterobacteriaceae is crucial.
  • Targeting epithelial cell metabolism presents a potential intervention strategy to control CPE spread.