Send to

Choose Destination
See comment in PubMed Commons below
FEMS Microbiol Lett. 2003 Nov 21;228(2):159-66.

Shiga toxins and apoptosis.

Author information

  • 1Department of Medical Microbiology and Immunology, Texas A&M University System Health Science Center, College Station, TX 77843-1114, USA.


The enteric pathogens Shigella dysenteriae serotype 1 and Shiga toxin-producing Escherichia coli (STEC) cause bloody diarrheal diseases that may progress to life-threatening extraintestinal complications. Although the S. dysenteriae and STEC differ in the expression of a number of virulence determinants, they share the capacity to produce one or more potent cytotoxins, called Shiga toxins (Stxs). Following the ingestion of the organisms, the expression of Stxs is critical for the development of vascular lesions in the colon, kidneys and central nervous system. It has been known for some time that following the intracellular routing of Stxs to the endoplasmic reticulum and nuclear membrane, the toxins translocate into the cytoplasm and target ribosomes for damage. However, numerous recent studies have shown that Stxs trigger programmed cell death signaling cascades in intoxicated cells. The mechanisms of apoptosis induction by these toxins are newly emerging, and the data published to date suggest that the toxins may signal apoptosis in different cells types via different mechanisms. Here we review the Stxs and the known mechanistic aspects of Stx-induced apoptosis, and present a model of apoptosis induction.

[PubMed - indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire
    Loading ...
    Support Center