Studies on the biological activities and emetic mechanism of staphylococcal enterotoxins

Staphylococcus aureus food poisoning was shown by Dack et al. in 1930 to be caused by staphylococcal enterotoxin (SE) produced by S. aureus, rather than by the bacterial infection. However, the emetic mechanism of SE has remained unclear. In this study, we analyzed the emetic activity of SE in several emetic animal models and tried to elucidate the mechanism of emesis. We established a small primate, common marmoset, as a novel emetic model for SE. We also analyzed the immunofluorescence analysis of the gastrointestinal tract of the common marmoset and found that SE binds to submucosal mast cells in the gastrointestinal tract and SE induces degranulation of the mast cells. Furthermore, we showed that SE induces histamine releases, which is inhibited by mast cell stabilizer. In addition, treatment of common marmosets with either mast cell stabilizer or histamine H1 receptor antagonists suppressed the emetic response induced by SE. These results indicate that orally administered SE binds to submucosal mast cells in the gastrointestinal tract and causes degranulation, resulting in the release of histamine, which in turn causes emesis.