Program IV. Interactions of Select Agent and Emerging Bacterial Pathogen Toxins with Host Cells
Shepherds: Alison O'Brien, Erik Hewlett
Shiga toxin and ricin interaction with enterocytes and rescue of target cells
Shiga toxin (Stx) of Shigella dysenteriae type 1, Stx1 and Stx2 of Escherichia coli O157:H7, and other Shiga toxin-producing E. coli (STEC), and ricin from the castor bean plant cause depurination of a critical residue in the 28S rRNA of 60S ribosomes and, hence, inhibition of protein synthesis, apoptosis, and cell death.
Early Interaction between Clostridium perfringens epsilon toxin and host cells
Clostridium perfringens epsilon toxin (ETX) is a class B CDC/USDA overlap toxin and a major virulence factor in natural veterinary infections caused by ETX-producing C. perfringens isolates. Currently there are no ETX therapeutics (NIH prefers ETX therapeutics over vaccines because natural ETX-related disease in humans is uncommon).
Integrated analysis of cellular responses to toxins from clostridium difficile
C. difficile colitis is a toxin-mediated disease, which is dependent on the actions of Toxin A (TcdA) and/or Toxin B (TcdB). Although the molecular mechanisms by which TcdA and TcdB modify Rho-subfamily GTPases are well defined, the pathways connecting those events to colitis and inflammatory diarrhea remain elusive.
Novel peptide antagonist therapy for superantigen-induced lethal shock
Bacterial superantigens (SAg) are exotoxins that trigger an excessive immune response that may lead to lethal shock. Because of their ability to induce incapacitation at exceedingly low concentrations and to elicit shock, their ease of production and their exceptional stability, SAgs are classified as Category B biological weapons.