The manipulation of cell signaling and host cell biology by cholera toxin

Vibrio cholerae colonizes the small intestine and releases cholera toxin into the extracellular space. The toxin binds to the apical surface of the epithelium, is internalized into the host endomembrane system, and escapes into the cytosol where it activates the stimulatory alpha subunit of the hete...

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Bibliographic Details
Published in:Cellular signalling 2022-12, Vol.100, p.110489-110489, Article 110489
Main Authors: White, Christopher, Bader, Carly, Teter, Ken
Format: Article
Language:English
Subjects:
ADP-ribosyl hydrolase
cAMP
Chlorides - metabolism
Cholera Toxin - genetics
Cholera Toxin - metabolism
Cholera Toxin - pharmacology
Cystic fibrosis transmembrane regulator
Endoplasmic Reticulum-Associated Degradation
GTP-Binding Proteins - metabolism
Lipid rafts
Molecular ratchet
Signal Transduction
Unfolded protein response
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Summary:Vibrio cholerae colonizes the small intestine and releases cholera toxin into the extracellular space. The toxin binds to the apical surface of the epithelium, is internalized into the host endomembrane system, and escapes into the cytosol where it activates the stimulatory alpha subunit of the heterotrimeric G protein by ADP-ribosylation. This initiates a cAMP-dependent signaling pathway that stimulates chloride efflux into the gut, with diarrhea resulting from the accompanying osmotic movement of water into the intestinal lumen. G protein signaling is not the only host system manipulated by cholera toxin, however. Other cellular mechanisms and signaling pathways active in the intoxication process include endocytosis through lipid rafts, retrograde transport to the endoplasmic reticulum, the endoplasmic reticulum-associated degradation system for protein delivery to the cytosol, the unfolded protein response, and G protein de-activation through degradation or the function of ADP-ribosyl hydrolases. Although toxin-induced chloride efflux is thought to be an irreversible event, alterations to these processes could facilitate cellular recovery from intoxication. This review will highlight how cholera toxin exploits signaling pathways and other cell biology events to elicit a diarrheal response from the host.
ISSN:0898-6568
1873-3913
DOI:10.1016/j.cellsig.2022.110489