Exotoxin

Other systems for classifying or identifying toxins include: The same exotoxin may have different names, depending on the field of research.

The best-characterized superantigens are those produced by the strains of Staphylococcus aureus and Streptococcus pyogenes that cause toxic shock syndrome.

As a consequence, up to 50% of all T cells are activated, leading to massive secretion of proinflammatory cytokines, which produce the symptoms of toxic shock.

Some strains of E. coli produce heat-stable enterotoxins (ST), which are small peptides that are able to withstand heat treatment at 100 °C.

For example, STa enterotoxins bind and activate membrane-bound guanylate cyclase, which leads to the intracellular accumulation of cyclic GMP and downstream effects on several signaling pathways.

The CDCs Streptococcus pneumoniae Pneumolysin, Clostridium perfringens perfringolysin O, and Listeria monocytogenes listeriolysin O cause specific modifications of histones in the host cell nucleus, resulting in down-regulation of several genes that encode proteins involved in the inflammatory response.

RTX toxins can be identified by the presence of a specific tandemly repeated nine-amino acid residue sequence in the protein.

(Ribosome structure is one of the most important differences between eukaryotes and prokaryotes, and, in a sense, these exotoxins are the bacterial equivalent of antibiotics such as clindamycin.)

[9] Vaccination with the toxoids generates antibodies against the exotoxins, forming immunological memory as protection against subsequent infections.

[11] The cancer cell is killed once the toxin is internalized;[11] for example, Pseudomonas exotoxin disrupts protein synthesis after cellular uptake.

[12] Multiple versions of recombinant exotoxin A, secreted by Pseudomonas aeruginosa, have entered clinical trials against tumor growth but have yet to be approved by Food and Drug Administration (FDA).

[12] A recombinant diphtheria exotoxin has been approved by the FDA for treatment of cutaneous T-cell lymphoma, an immune system cancer.

This figure shows that exotoxins are secreted by bacterial cells, Clostridium botulinum for example, and are toxic to somatic cells. Somatic cells have antibodies on the cell wall to target exotoxins and bind to them, preventing the invasion of somatic cells. The binding of the exotoxin and antibody forms an antigen-antibody interaction and the exotoxins are targeted for destruction by the immune system. If this interaction does not happen, the exotoxins bind to the exotoxin receptors that are on the cell surface and causes death of the host cell by inhibiting protein synthesis. This figure also shows that the application of heat or chemicals to exotoxins can result in the deactivation of exotoxins. The deactivated exotoxins are called toxoids and they are not harmful to somatic cells.