@article{oai:hirosaki.repo.nii.ac.jp:00003710,
 author = {Hu, Dong-Liang and Omoe, Katsuhiko and Sashinami, Hiroshi and Shinagawa, Kunihiro and Nakane, Akio},
 issue = {Supplement},
 journal = {弘前医学},
 month = {Jul},
 note = {Background. Staphylococcal enterotoxins （SEs） are the most common cause of food-borne diseases and toxic shock syndrome throughout the world. However, little is known about the mechanism of emesis induced by SEs and no vaccine that prevents SE-induced emesis has been described. Methods. A nontoxic mutant SEA, SEAD227A, was constructed by site-directed mutagenesis and purified from Escherichia coli expression system. House musk shrews, a small emetic animal model, were immunized with SEAD227A and then challenged with wild-type SEA. SEA-induced emesis was recorded for 3 h. Antibody production was analyzed by gel double-immunodiff usion assay. Neutralizing activities of the antibodies to superantigenic and emetic activities were analyzed in vitro and in vivo. Results. SEAD227A was devoid of both superantigenic and emetic activities, but still retained its immunological activity. Immunization with SEAD227A strongly induced specifi c antibody production and signifi cantly provided the protection against SEA-induced emesis. The antibodies from immunized shrews markedly inhibited the SEA-induced proliferation of spleen cells and also significantly ablated the SEA-induced vomiting in the animals. Conclusions. These results suggest that vaccination with SEAD227A devoid of toxic properties provides protection against SEAinduced emesis. This nontoxic mutant and its specifi c antibodies might be useful in the prevention and treatment of staphylococcal food poisoning, 弘前医学. 61(Suppl.), 2010, p.S215-S223},
 pages = {S215--S223},
 title = {＜Poster＞Cystatin C immunoreactivity and neuronal degeneration in amyotrophic lateral sclerosis},
 volume = {61},
 year = {2010}
}