Citation

Lin CF, Chen CL, Huang WC, Cheng YL, Hsieh CY, Wang CY, Hong MY. Toxins (Basel) 2010; 2(8): 2158-2176.

Affiliation

Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan; Email: zarbi@mail2000.com.tw (W.-C.H.); sillylilly0518@yahoo.com.tw (Y.-L.C.); dyoushus@yahoo.com.tw (C.-Y.H.); chixuan1225@hotmail.com (C.-Y.W.); myuan@mail2000.com.tw (M.-Y.H.).

Copyright

(Copyright © 2010, MDPI: Multidisciplinary Digital Publishing Institute)

DOI

10.3390/toxins2082158

PMID

22069678

PMCID

PMC3153280

Abstract

The infection of bacterial organisms generally causes cell death to facilitate microbial invasion and immune escape, both of which are involved in the pathogenesis of infectious diseases. In addition to the intercellular infectious processes, pathogen-produced/secreted enterotoxins (mostly exotoxins) are the major weapons that kill host cells and cause diseases by inducing different types of cell death, particularly apoptosis and necrosis. Blocking these enterotoxins with synthetic drugs and vaccines is important for treating patients with infectious diseases. Studies of enterotoxin-induced apoptotic and necrotic mechanisms have helped us to create efficient strategies to use against these well-characterized cytopathic toxins. In this article, we review the induction of the different types of cell death from various bacterial enterotoxins, such as staphylococcal enterotoxin B, staphylococcal alpha-toxin, Panton-Valentine leukocidin, alpha-hemolysin of Escherichia coli, Shiga toxins, cytotoxic necrotizing factor 1, heat-labile enterotoxins, and the cholera toxin, Vibrio cholerae. In addition, necrosis caused by pore-forming toxins, apoptotic signaling through cross-talk pathways involving mitochondrial damage, endoplasmic reticulum stress, and lysosomal injury is discussed.

Language: en