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Pushing boundaries: mechanisms enabling bacterial pathogens to spread between cells.

Julie E Raab1, Desmond J Hamilton1, Tucker B Harju1

  • 1Department of Immunology and Microbiology, School of Medicine, University of Colorado-Anschutz Medical Campus, Denver, Colorado, USA.

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Intracellular bacteria like Shigella use host cell actin to form membrane protrusions for spreading. This review details how these structures form and resolve, aiding bacterial intercellular movement and disease.

Keywords:
BurkholderiaListeriaRickettsiaShigellaactinintercellular spreadprotrusions

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Area of Science:

  • Microbiology
  • Cell Biology
  • Pathogenesis

Background:

  • Intracellular bacterial pathogens spread between host cells, a key step in human disease.
  • Pathogens like Shigella, Listeria, Rickettsia, and Burkholderia manipulate host actin cytoskeleton for cell-to-cell spread.
  • This process involves forming membrane protrusions that extend into adjacent cells.

Purpose of the Study:

  • To review the mechanisms of intercellular spread utilized by intracellular bacterial pathogens.
  • To highlight the interactions between bacterial and host factors driving this spread.
  • To focus on the formation and resolution of protrusion structures during intercellular movement.

Main Methods:

  • Literature review of recent research on bacterial intercellular spread.
  • Analysis of host-pathogen interactions.
  • Focus on actin cytoskeleton manipulation and membrane protrusion dynamics.

Main Results:

  • Intracellular bacteria hijack host actin to create membrane protrusions for cell entry.
  • Protrusions are resolved into double-membrane vacuoles (DMVs) from which bacteria escape.
  • Bacterial escape into the cytosol allows for repeated rounds of intercellular spread.

Conclusions:

  • Understanding protrusion formation and resolution is crucial for deciphering bacterial pathogenesis.
  • Host-pathogen interactions governing actin dynamics are central to intercellular spread.
  • This mechanism is vital for the dissemination of multiple significant intracellular bacterial pathogens.