Lymphoproliferative activity of Pseudomonas exotoxin A is dependent on intracellular processing and is associated with the carboxyl-terminal portion.

Pseudomonas aeruginosa exotoxin A (PE) represents a microbial superantigen that requires processing by accessory cells in order to induce the proliferation of V beta 8-bearing murine T lymphocytes. In this study, we have observed that PE requires intracellular processing by a protease in order to induce lymphoproliferation. Pepstatin A, an inhibitor of acid proteases, inhibited PE-induced lymphoproliferation, whereas leupeptin, an inhibitor of serine and thiol proteases, had no effect on PE-induced lymphoproliferation.

The superantigen Pseudomonas exotoxin A requires additional functions from accessory cells for T lymphocyte proliferation.

We have examined the functions required of accessory cells (AC) for murine thymocyte proliferation induced by Pseudomonas exotoxin A (PE) and have compared these functions to those required of a known superantigen, staphylococcal enterotoxin B (SEB). We demonstrate that PE, like SEB, preferentially stimulates PNA+ thymocytes expressing a specific V beta element within the T cell receptor. However, PE requires functions from AC that are distinct from those required by SEB.

Induction of interleukin-1 from murine peritoneal macrophages by Pseudomonas aeruginosa exotoxin A.

Pseudomonas exotoxin A, an ADP-ribosylating toxin produced by Pseudomonas aeruginosa, has been shown to stimulate the proliferation of murine thymocytes, which requires the participation of accessory cells. This requirement for accessory cells can be replaced by supernatant from adherent peritoneal exudate cells that have been stimulated with exotoxin A. Antibody to exotoxin A inhibits the induction of the thymocyte mitogenic activity from adherent peritoneal macrophages.