Enterotoxin

Source: Wikipedia, the free encyclopedia.
Staph/Strep enterotoxin, C terminal
SCOP2
1se3 / SCOPe / SUPFAM
OPM superfamily364
OPM protein1dyq
Available protein structures:
Pfam  structures / ECOD  
PDBRCSB PDB; PDBe; PDBj
PDBsumstructure summary

An enterotoxin is a

cell membranes
. This causes the cells to die.

Clinical significance

Enterotoxins have a particularly marked effect upon the

osmolarity of the luminal contents of the intestines. Increased chloride permeability leads to leakage into the lumen followed by sodium and water movement. This leads to a secretory diarrhea within a few hours of ingesting enterotoxin. Several microbial organisms contain the necessary enterotoxin to create such an effect, such as Staphylococcus aureus and E. coli.[3]

The drug linaclotide, used to treat some forms of constipation, is based on the mechanism of enterotoxins.[3]

Classification and 3D structures

Bacterial

Enterotoxins can be formed by the bacterial pathogens Staphylococcus aureus and Bacillus cereus and can cause

toxic shock syndrome toxin, which shares only a low level of sequence
similarity with this group.

All of these toxins share a similar two-domain

binding mode(s) when it interacts with MHC class II molecules or the T-cell receptor.[9]

The beta-grasp domain has some

SCOP database
.

Viral

Viruses in the families

Astroviridae are responsible for a huge percentage of gastrointestinal disease worldwide. Rotaviruses (of Reoviridae) have been found to contain an enterotoxin which plays a role in viral pathogenesis. NSP4, is a protein that is made during the intracellular phase of the virion's life cycle and is known to have a primary function in intracellular virion maturation.[13] However, when NSP4 from group A Rotaviruses was purified (4 alleles tested), concentrated, and injected into a mouse model, diarrheal disease mimicking that caused by Rotavirus infection commenced.[14] A putative mode of toxicity is that NSP4 activates a signal transduction pathway that ultimately results in an increased cellular concentration of calcium and subsequent chloride secretion from the cell.[15]
Secretion of ions from villi lining the gut alter normal osmotic pressures and prevent uptake of water, eventually causing diarrhea.

See also

References

External links