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Updated: Jul 28, 2025

Immunometabolic Circuits in Infection for Advancing Host Directed Therapies
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Immunometabolic Circuits in Infection for Advancing Host Directed Therapies

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Attaching and effacing pathogens modulate host mitochondrial structure and function.

Anusha Harishankar1, V K Viswanathan2

  • 1School of Animal and Comparative Biomedical Sciences, The University of Arizona, Tucson, AZ, United States.

International Review of Cell and Molecular Biology
|June 2, 2023
PubMed
Summary
This summary is machine-generated.

Enteropathogenic and enterohemorrhagic Escherichia coli use a type III secretion system to deliver effectors that alter host cell mitochondria. Understanding these mitochondrial effects is key to deciphering bacterial pathogenesis and developing treatments.

Keywords:
Attaching-effacing (A/E) pathogensCell deathCitrobacter rodentiumEPECIntestinal epitheliumMitochondrial membrane potentialMitochondrial morphologyOxidative phosphorylationType 3 secretion system

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Area of Science:

  • Microbiology
  • Cell Biology
  • Pathogenesis

Background:

  • Enteropathogenic (EPEC) and enterohemorrhagic (EHEC) Escherichia coli are significant human enteric pathogens.
  • These bacteria, along with Citrobacter rodentium, are "attaching and effacing" (A/E) pathogens that utilize a type III secretion system (T3SS).
  • The T3SS delivers effector proteins into host cells, crucial for bacterial colonization and disease.

Purpose of the Study:

  • To provide an overview of host cell alterations induced by A/E pathogens.
  • To specifically focus on the impact of bacterial effectors on host cell mitochondria.
  • To highlight the critical role of mitochondria in A/E bacterial pathogenesis.

Main Methods:

  • Review of in vitro studies detailing effector interactions with mitochondria.
  • Analysis of in vivo studies, primarily using the Citrobacter rodentium/mouse model.
  • Examination of host cell modifications, including mitochondrial morphology, function, and apoptosis.

Main Results:

  • Bacterial effectors directly target mitochondria, altering morphology, oxidative phosphorylation, and ROS production.
  • Disruption of mitochondrial membrane potential and induction of intrinsic apoptosis are observed.
  • In vivo studies confirm some in vitro findings and suggest broader physiological changes in the intestine.

Conclusions:

  • Mitochondrial modifications are a central mechanism by which A/E pathogens cause disease.
  • Deciphering effector-mitochondria interactions is essential for understanding pathogenesis.
  • Further research is needed to define the mechanistic underpinnings of in vivo mitochondrial alterations.