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Sustained exposure to outer membrane vesicles from Escherichia coli develop mitochondrial oxidative stress and induce

Deng Siqian1,2, Wang Yingjie1,2, Chen Guangzhang3

  • 1School of Basic Medicine, Bengbu Medical University, Bengbu, 233030, China.

Archives of Microbiology
|May 13, 2026
PubMed

Insights

Escherichia coli outer membrane vesicles (OMVs) enter macrophages, delivering cargo that causes mitochondrial dysfunction and inflammation. These findings reveal how E. coli uses OMVs to impact host-pathogen interactions.

Area of Science:

  • Microbiology
  • Immunology
  • Cell Biology

Background:

  • Escherichia coli release outer membrane vesicles (OMVs) carrying virulence and immunomodulatory factors.
  • OMVs play a role in host-pathogen interactions during infection.

Purpose of the Study:

  • To investigate the interaction of E. coli OMVs with Raw 264.7 macrophages.
  • To determine the cellular effects and molecular mechanisms of E. coli OMVs.

Main Methods:

  • Isolation and characterization of E. coli OMVs.
  • Macrophage cell culture and treatment with OMVs.
  • Electron microscopy for cellular uptake visualization.
  • Assessment of cell viability, reactive oxygen species (ROS) levels, autophagy, and ATP levels.
  • Measurement of proinflammatory cytokine production.

Main Results:

  • E. coli OMVs were readily internalized by Raw 264.7 macrophages and localized within the cytoplasm and membrane vesicles.
  • OMVs were non-toxic to macrophages within the tested concentration range (1-10 µg/mL).
  • OMVs targeted macrophage mitochondria, leading to increased ROS, activated autophagy, and reduced ATP levels, indicating mitochondrial dysfunction.
  • E. coli OMVs induced significant, dose-dependent proinflammatory responses in macrophages.

Conclusions:

  • E. coli utilizes OMVs to deliver virulence factors and immunomodulatory proteins to host cells.
  • OMV uptake triggers mitochondrial dysfunction, autophagy, and inflammatory responses in macrophages.
  • These mechanisms contribute to the modulation of host-pathogen interactions during E. coli infections.
Keywords:
Escherichia coliAutophagyMacrophage cellsMitochondriaOuter membrane vesicles

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