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Ricin and Shiga toxins: effects on host cell signal transduction

Dakshina M Jandhyala1, Cheleste M Thorpe, Bruce Magun

  • 1Tufts University School of Medicine, Tufts Medical Center, 800 Washington Street, Box 041, Boston, MA 02111, USA. djandhyala@tuftsmedicalcenter.org

Current Topics in Microbiology and Immunology
|November 8, 2011
PubMed

Insights

Shiga toxins and ricin inhibit protein synthesis and trigger inflammatory responses. This review details the signaling pathways activated by these potent toxins, contributing to disease pathogenesis.

Area of Science:

  • Toxicology
  • Molecular Biology
  • Cellular Signaling

Background:

  • Shiga toxins and ricin are highly toxic proteins.
  • These toxins inhibit crucial cellular protein synthesis.
  • They also activate inflammatory pathways linked to severe disease.

Purpose of the Study:

  • To review the signaling pathways activated by Shiga toxins and ricin.
  • To understand the role of these pathways in toxin-induced diseases.

Main Methods:

  • Literature review of cellular and molecular studies.
  • Analysis of signaling cascades involved in toxin intoxication.

Main Results:

  • Shiga toxins and ricin activate multiple stress and inflammatory pathways.
  • Key pathways include ribotoxic stress, NF-κB, inflammasome, UPR, and mTOR signaling.
  • Toxin effects on hemostasis and retrograde trafficking are also discussed.

Conclusions:

  • Understanding these signaling pathways is critical for elucidating toxin pathogenesis.
  • This knowledge may inform therapeutic strategies against Shiga toxin and ricin poisoning.

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