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Shiga Toxin 2a Induces NETosis via NOX-Dependent Pathway.

Wouter J C Feitz1,2, Samuel Suntharalingham2,3, Meraj Khan3

  • 1Department of Pediatric Nephrology, Amalia Children's Hospital, Radboud Institute for Molecular Life Sciences, Radboudumc, 6525 GA Nijmegen, The Netherlands.

Biomedicines
|December 24, 2021
PubMed
Summary
This summary is machine-generated.

Shiga toxin (Stx) from E. coli causes hemolytic uremic syndrome (HUS). This study shows Stx2a triggers neutrophil extracellular trap (NET) formation via the NOX-dependent pathway, contributing to HUS pathogenesis.

Keywords:
NADPH-oxidase-dependent pathwaySTEC-HUShemolytic uremic syndromeneutrophil extracellular trapsshiga toxin

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Area of Science:

  • Immunology
  • Pathology
  • Microbiology

Background:

  • Shiga toxin (Stx)-producing Escherichia coli (STEC) infection is a primary cause of hemolytic uremic syndrome (HUS), a leading cause of acute kidney injury in children.
  • Stx is implicated in STEC-HUS pathogenesis and endothelium damage, but its precise effects on neutrophils and neutrophil extracellular trap (NET) formation remain unclear.

Purpose of the Study:

  • To investigate the impact of Stx2a on NET formation and associated pathways (NOX-dependent and -independent).
  • To compare NETosis in neutrophils from healthy donors and STEC-HUS patients during acute and recovery phases.

Main Methods:

  • Isolated neutrophils from healthy donors and STEC-HUS patients (acute and recovery phases).
  • Stimulated neutrophils with Stx2a and assessed NET formation.
  • Utilized pathway-specific inhibitors (DPI, ERK, P38) to elucidate NETosis mechanisms.
  • Measured reactive oxygen species (ROS) production.

Main Results:

  • Stx2a induced NETosis in a dose-dependent manner in neutrophils from both healthy controls and STEC-HUS patients.
  • Stx2a-induced NETosis occurred via the NOX-dependent pathway.
  • Neutrophils from STEC-HUS patients in the acute phase exhibited reduced ROS and NET formation compared to those in the recovery phase and healthy controls.

Conclusions:

  • Stx2a directly induces NETosis through the NOX-dependent pathway.
  • Altered neutrophil function in acute STEC-HUS may influence disease severity.
  • Stx2a-induced NETs could activate endothelial cells, potentially contributing to thrombotic microangiopathy in STEC-HUS.