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Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling
Published on: June 25, 2015
Induction of apoptosis by Shiga toxins
1Department of Microbial & Molecular Pathogenesis, College of Medicine, Texas A&M University System Health Science Center, 407 Reynolds Medical Building, College Station, TX 77843-1114, USA. tesh@medicine.tamhsc.edu
Abstract:
Shiga toxins comprise a family of structurally and functionally related protein toxins expressed by Shigella dysenteriae serotype 1 and multiple serotypes of Escherichia coli. While the capacity of Shiga toxins to inhibit protein synthesis by catalytic inactivation of eukaryotic ribosomes has been well described, it is also apparent that Shiga toxins trigger apoptosis in many cell types. This review presents evidence that Shiga toxins induce apoptosis of epithelial, endothelial, leukocytic, lymphoid and neuronal cells. Apoptotic signaling pathways activated by the toxins are reviewed with an emphasis on signaling mechanisms that are shared among different cell types. Data suggesting that Shiga toxins induce apoptosis through the endoplasmic reticulum stress response and clinical evidence demonstrating apoptosis in humans infected with Shiga toxin-producing bacteria are briefly discussed. The potential for use of Shiga toxins to induce apoptosis in cancer cells is briefly reviewed.
Insights
Shiga toxins from bacteria trigger programmed cell death (apoptosis) in various human cells. This review explores the mechanisms and potential therapeutic applications of Shiga toxin-induced apoptosis.
Area of Science:
- Microbiology
- Cell Biology
- Toxicology
Background:
- Shiga toxins are protein toxins produced by Shigella dysenteriae and Escherichia coli.
- These toxins are known to inhibit protein synthesis by inactivating ribosomes.
- Emerging evidence indicates Shiga toxins also induce apoptosis in numerous cell types.
Purpose of the Study:
- To review the evidence that Shiga toxins induce apoptosis across diverse cell types.
- To examine the shared apoptotic signaling pathways activated by these toxins.
- To discuss the role of endoplasmic reticulum stress and clinical implications.
Main Methods:
- Literature review of studies investigating Shiga toxin effects on cells.
- Analysis of apoptotic signaling pathways.
- Examination of endoplasmic reticulum stress response mechanisms.
Main Results:
- Shiga toxins induce apoptosis in epithelial, endothelial, leukocytic, lymphoid, and neuronal cells.
- Common signaling pathways are activated across different cell types.
- Endoplasmic reticulum stress is implicated in Shiga toxin-induced apoptosis.
Conclusions:
- Shiga toxins are potent inducers of apoptosis through conserved cellular mechanisms.
- Apoptosis is a significant factor in diseases caused by Shiga toxin-producing bacteria.
- Shiga toxins may hold potential for cancer therapy by inducing apoptosis in tumor cells.
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