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Author Spotlight: Advancements in Understanding and Combatting Shigella Infections
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Author Spotlight: Advancements in Understanding and Combatting Shigella Infections

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The type 3 secretion effector IpgD promotes S. flexneri dissemination

Volkan K Köseoğlu1, Marieke K Jones2, Hervé Agaisse1

  • 1Department of Microbiology, Immunology, and Cancer Biology, School of Medicine, University of Virginia, Charlottesville, Virginia, United States of America.

Plos Pathogens
|February 7, 2022
PubMed

Insights

Shigella flexneri uses the type 3 secretion system (T3SS) effector IpgD to spread between cells. IpgD reduces membrane protrusion resolution into double-membrane vacuoles, promoting bacterial dissemination and dysentery severity.

Area of Science:

  • Microbiology
  • Cell Biology
  • Infectious Diseases

Background:

  • Shigella flexneri causes significant global mortality and morbidity from bacillary dysentery.
  • Pathogenic Shigella invades epithelial cells and spreads via cell-to-cell transmission, a process involving actin-based motility and membrane protrusion formation.
  • The type 3 secretion system (T3SS) is crucial for Shigella dissemination, but its mechanisms remain unclear.

Purpose of the Study:

  • To elucidate the role of the T3SS effector IpgD in Shigella flexneri cell-to-cell spread.
  • To investigate how IpgD influences the formation and resolution of membrane structures during bacterial dissemination.
  • To determine the in vivo significance of IpgD in Shigella pathogenesis.

Main Methods:

  • Investigated the function of IpgD in mediating the resolution of membrane protrusions into double-membrane vacuoles (DMVs).
  • Assessed the enzymatic activity of IpgD as a phosphatidylinositol 4-phosphatase and its effect on PtdIns(4,5)P2 levels.
  • Utilized an infant rabbit model of shigellosis to evaluate the in vivo role of IpgD in dissemination and disease severity.

Main Results:

  • Demonstrated that IpgD facilitates the resolution of membrane protrusions into DMVs, a key step in Shigella cell-to-cell spread.
  • Showed that IpgD's phosphatase activity lowers PtdIns(4,5)P2 levels in protrusions, inhibiting actin polymerization that hinders DMV formation.
  • Confirmed that IpgD is essential for efficient in vivo dissemination and contributes to the severity of dysentery in a rabbit model.

Conclusions:

  • IpgD is a critical T3SS effector that promotes Shigella dissemination by regulating membrane dynamics and actin polymerization.
  • Targeting IpgD function could be a strategy to combat Shigella infections.
  • This study clarifies a key mechanism of Shigella pathogenesis and its contribution to disease severity.

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