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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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The induction of apoptosis by Shiga toxins and ricin

Vernon L Tesh1

  • 1Department of Microbial and Molecular Pathogenesis, College of Medicine, Texas A&M University Health Science Center, College Station, TX 77843-1114, USA. tesh@medicine.tamhsc.edu

Current Topics in Microbiology and Immunology
|December 2, 2011
PubMed

Insights

Shiga toxins and ricin inhibit protein synthesis and induce apoptosis. Non-enzymatic parts of these toxins can also trigger apoptosis, involving cell stress responses.

Area of Science:

  • Toxicology
  • Cell Biology
  • Molecular Biology

Background:

  • Shiga toxins and ricin are ribosome-inactivating proteins that inhibit protein synthesis.
  • These toxins are known to induce apoptosis across various cell types and organs.
  • Evidence suggests a dissociation between protein synthesis inhibition and apoptosis induction.

Purpose of the Study:

  • To review studies on Shiga toxin- and ricin-induced apoptosis.
  • To explore the signaling mechanisms underlying toxin-mediated apoptosis.
  • To examine the role of cell stress responses in toxin-induced apoptosis.

Main Methods:

  • Review of existing literature on Shiga toxins and ricin.
  • Analysis of studies investigating apoptosis pathways (extrinsic and intrinsic).
  • Examination of evidence for cell stress response involvement (ribotoxic stress response, unfolded protein response).

Main Results:

  • Shiga toxins and ricin inhibit protein synthesis by inactivating eukaryotic ribosomes.
  • Both toxins induce apoptosis in diverse cell types in vitro and in vivo.
  • Non-enzymatic toxin components can also induce apoptosis.
  • Toxins activate both extrinsic and intrinsic apoptosis pathways.
  • Cell stress response pathways, including the ribotoxic stress response and unfolded protein response, may be involved.

Conclusions:

  • Shiga toxins and ricin are potent inducers of apoptosis through multiple pathways.
  • The precise signaling mechanisms require further elucidation.
  • Cell stress responses are implicated in the apoptotic effects of these toxins.

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