AB5 toxin

The AB5 toxins are six-component protein complexes secreted by certain pathogenic bacteria known to cause human diseases such as cholera, dysentery, and hemolytic-uremic syndrome. One component is known as the A subunit, and the remaining five components are B subunits. All of these toxins share a similar structure and mechanism for entering targeted host cells. The B subunit is responsible for binding to receptors to open up a pathway for the A subunit to enter the cell. The A subunit is then able to use its catalytic machinery to take over the host cell's regular functions. The AB5 toxins are six-component protein complexes secreted by certain pathogenic bacteria known to cause human diseases such as cholera, dysentery, and hemolytic-uremic syndrome. One component is known as the A subunit, and the remaining five components are B subunits. All of these toxins share a similar structure and mechanism for entering targeted host cells. The B subunit is responsible for binding to receptors to open up a pathway for the A subunit to enter the cell. The A subunit is then able to use its catalytic machinery to take over the host cell's regular functions. There are four main families of the AB5 toxin. These families are characterized by the sequence of their A (catalytic) subunit, as well as their catalytic ability. This family is also known as Ct or Ctx, and also includes the heat-labile enterotoxin, known as LT. Cholera toxin’s discovery is credited by many to Dr. Sambhu Nath De. He conducted his research in Calcutta (now Kolkata) making his discovery in 1959, although it was first purified by Robert Koch in 1883. Cholera toxin is composed of a protein complex that is secreted by the bacterium Vibrio cholerae. Some symptoms of this toxin include chronic and widespread watery diarrhea and dehydration that, in some cases, leads to death. This family is also known as Ptx and contains the toxin responsible for whooping cough. Pertussis toxin is secreted by the gram-negative bacterium, Bordetella pertussis. Whooping cough is very contagious and cases are slowly increasing in the United States despite vaccination. Symptoms include paroxysmal cough with whooping and even vomiting. The bacterium Bordetella pertussis was first identified as the cause of whooping cough and isolated by Jules Bordet and Octave Gengou in France in 1900. The toxin shares its mechanism with cholera toxin. ArtAB toxin of Salmonella enterica has components similar to those found in two different families: the ArtA (Q404H4) subunit is homologous with pertussis toxin A, while the ArtB (Q404H3) subunit is homologous with subB as well as proteins found in other Salmonella strains. Under the categorize-by-A rule, it is a Ptx-family toxin. Shiga toxin, also known as Stx, is a toxin that is produced by the rod shaped Shigella dysenteriae and Escherichia coli (STEC). Food and drinks contaminated with these bacteria are the source of infection and how this toxin is spread. Symptoms include abdominal pain as well as watery diarrhea. Severe life-threatening cases are characterized by hemorrhagic colitis (HC). The discovery of shiga toxin is credited to Dr. Kiyoshi Shiga in 1898. This family is also known as SubAB and was discovered during the 1990s. It produced by strains of STEC that do not have the locus of enterocyte effacement (LEE), and is known to cause hemolytic-uremic syndrome (HUS). It is called a subtilase cytotoxin because its A subunit sequence is similar to that of a subtilase-like serine protease in Bacillus anthracis. Some symptoms caused by this toxin are a decrease in platelet count in the blood or thrombocytopenia, an increase in white blood cell count or leukocytosis, and renal cell damage. The subtilase cytotoxin A subunit (subA, Q6EZC2) is a protease known to cleave binding immunoglobulin protein (BiP), leading to endoplasmic reticulum stress and cell death. The B subunits (subB, Q6EZC3) bind to N-Glycolylneuraminic acid (Neu5Gc) glycans on cells with high affinity. Just subB is sufficient to cause vacuolation of vero cells. Neu5GC is not made by humans but is acquired from food sources such as red meat and dairy products, also frequent sources of STEC infections, into the human gut lining.