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Virulent Shigella flexneri causes damage to mitochondria and triggers necrosis in infected human monocyte-derived

James F Koterski1, Massoumeh Nahvi, Malabi M Venkatesan

  • 1Department of Surgery and the Cancer Institute of New Jersey, RWJMS-UMDNJ, New Brunswick, NJ 08903, USA.

Infection and Immunity
|December 25, 2004
PubMed

Insights

Shigella flexneri infection rapidly increases human monocyte-derived macrophage (HMDM) cell membrane permeability and depletes ATP. This bacterium targets host cell mitochondria, leading to their destruction and subsequent necrotic cell death.

Area of Science:

  • Microbiology
  • Cell Biology
  • Immunology

Background:

  • Shigella flexneri causes bacillary dysentery, characterized by acute colon inflammation.
  • The impact of virulent Shigella infection on phagocytes, particularly macrophages, is not fully understood.

Purpose of the Study:

  • To investigate the effects of virulent Shigella flexneri on human monocyte-derived macrophages (HMDM) and monocytes.
  • To determine the mechanism by which Shigella induces cell death in infected macrophages.

Main Methods:

  • In vitro infection of HMDM and monocytes with virulent Shigella flexneri.
  • Assessment of cell membrane permeability using fluorescent vital dyes (propidium iodide).
  • Measurement of intracellular ATP levels and mitochondrial membrane potential.

Main Results:

  • Virulent Shigella rapidly increased cell membrane permeability in HMDM (59%) but not monocytes (
  • Infected HMDM showed a significant drop in ATP levels (approx. 50%).
  • Loss of mitochondrial membrane potential preceded cell membrane permeability increase, indicating mitochondrial targeting.

Conclusions:

  • Virulent Shigella flexneri specifically targets and destroys mitochondria in HMDM.
  • Mitochondrial destruction by Shigella is a key event leading to necrotic cell death in macrophages.
  • This mechanism contributes to the pathogenesis of Shigella-induced dysentery.

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