Anaphylaxis is an acute systemic allergic reaction (severe type I hypersensitivity) to a specific allergen and occurs in human and other mammals. Food anaphylaxis is most frequently triggered by peanut, buckwheat, milk, egg, and wheat allergens. Anaphylactic mouse models against ovalbumin and peanut allergens have been established by repeated exposure to small amounts of allergen with adjuvant via subcutaneous (s.c.) and intraperitoneal (i.p.) routes. When immunity is established, the animals are challenged with a large quantity of allergens via an i.v. route to induce anaphylaxis. However, i.v. sensitization is a relatively complicated procedure, and establishing an anaphylactic model requires considerable time. In addition, the i.p. method for allergen delivery is simpler than i.v. routes, has lower risk for failure, and can shorten sensitization duration. Here, we attempted to develop a simple anaphylactic shock model by exposing mice to a B-type CpG-oligodeoxynucleotide (ODN), termed MsST, which had the immune ability to induce IL-33 and IFN-γ production from the lac Z gene of Streptococcus thermophilus ATCC19258 with allergen via an i.p. route. After the allergen challenge for inducing anaphylactic shock, IgG_2a-production and IFN-γ-positive cells were markedly increased in mice that received B-type CpG-ODN. In contrast, IL-33-positive cells in the model mice were only slightly increased. Generally, IFN-γ supports Th1 cell responses that suppress allergic disease. However, it was previously reported that IFN-γ enhances platelet-activating factor, which is a bioactive lipid mediator that plays a role in the onset of inflammatory diseases such as asthma, anaphylaxis and atherosclerosis, and is involved in the generation of CD11b⁺ and CD11c⁺ cells. The anaphylactic shock model described here is expected to contribute to the development of anaphylaxis treatment strategies.