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Endothelial damage induced by Shiga toxins delivered by neutrophils during transmigration

Maurizio Brigotti1, Pier Luigi Tazzari, Elisa Ravanelli

  • 1Dipartimento di Patologia Sperimentale, Università di Bologna, Bologna, Italy. maurizio.brigotti@unibo.it

Journal of Leukocyte Biology
|April 8, 2010
PubMed

Insights

Shiga toxin (Stx) binding to neutrophils (PMN) facilitates toxin transfer to endothelial cells, causing damage. Low toxin doses trigger inflammation, while high doses cause cell death, suggesting a self-amplifying cycle in HUS.

Area of Science:

  • Nephrology
  • Immunology
  • Microbiology

Background:

  • Shiga toxin (Stx) from STEC infections causes endothelial damage, a key factor in human hemolytic uremic syndrome (HUS).
  • The role of polymorphonuclear neutrophils (PMN) in transporting Stx during HUS pathogenesis has been debated.

Purpose of the Study:

  • To investigate the role of PMN as carriers of Stx1 and their contribution to endothelial damage in HUS.
  • To elucidate the effects of Stx1-loaded PMN on endothelial cells, focusing on toxin transfer and subsequent cellular responses.

Main Methods:

  • Confirmation of Stx1 binding to PMN and assessment of its degranulating effects.
  • Utilizing a two-chamber transmigration device to model PMN carrying varying Stx1 loads migrating through endothelial cell monolayers.
  • Analysis of endothelial cell protein synthesis, cytokine production, and apoptosis following Stx1 transfer from transmigrating PMN.

Main Results:

  • PMN bind Stx1 and exhibit degranulation.
  • Transmigrating PMN successfully transferred Stx1 to endothelial cells, impairing protein synthesis and inducing proinflammatory cytokine release.
  • Low Stx1 doses on PMN stimulated high cytokine release, while high doses led to translation impairment and apoptosis in endothelial cells.

Conclusions:

  • PMN act as carriers for Stx1, facilitating its transfer to renal endothelial cells.
  • A self-amplifying inflammatory loop, initiated by low-dose Stx transfer via PMN, may drive renal damage in HUS.
  • The dose of Stx carried by PMN significantly influences the outcome of endothelial cell response, ranging from inflammation to apoptosis.

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