ANTIGEN-INDUCED ANAPHYLACTIC DEATH IN MICE

Intravenous injection of bovine serum albumin (BSA) into the BSA/CFA-p rimed ICR mice specifically induced anaphylactic death within 1 h. The anaphylactic death could not be induced until day 8 after sensitizati on, and sensitization subsisted for more than 3 months. The response w as dose dependent; mice challenged with BSA doses higher or equivalent to 25 mu g developed anaphylactic death. The intravenous route was mo re effective than the intraperitoneal one, while subcutaneous injectio n was ineffective. Antigen in any of complete Freund's adjuvant, incom plete Freund's adjuvant or aluminum hydroxide could sensitize the mice to develop anaphylactic death. The combination of antigen and the mou se strain or the gender of the mouse determined the susceptibility of the anaphylactic death. AKR, B10.BR, as well as ICR, strains were susc eptible. Antigen of HoGG induced a higher mortality rate than that of GAT or lysozyme. Male mice were more susceptible than female ones. The BSA-induced anaphylactic death could be prevented by pretreating ICR mice with cyproheptadine (histamine and serotonin antagonist) or diphe nhydramine (histamine antagonist) and ketanserin (serotonin antagonist ). Intravenous injection of saline during anaphylaxis also protected t he mice from death. Furthermore, immune serum could transfer the anaph ylactic death, and heat (56 degrees C, 4 h) did not destroy its activi ty. The primary IgG subclass induced by GAT, HoGG or lysozyme was IgG1 . There was no qualitative difference in the IgG subclass induced in d ifferent strains by different antigens. The IgE class of antibodies wa s not detectable. These results suggest that there is a non-IgE-mediat ed anaphylactic death which involves the release of histamine and sero tonin that cause the increase of vasopermeability and fatal blood volu me loss.