Nasal exposure to Staphylococcal enterotoxin enhances the development of allergic rhinitis in mice

• Published in: Clinical and experimental allergy 2005-04, Vol.35 (4), p.506-514
• Main Authors: Okano, M., Hattori, H., Yoshino, T., Sugata, Y., Yamamoto, M., Fujiwara, T., Satoskar, A. A., Satoskar, A. R., Nishizaki, K.
• Format: Article
• Language: English
• Subjects: Allergens - immunology; Allergic diseases; allergy; Animals; Antibody Specificity - immunology; Biological and medical sciences; Cells, Cultured; Dose-Response Relationship, Immunologic; enterotoxin; Enterotoxins - immunology; Eosinophilia - immunology; Female; Fundamental and applied biological sciences. Psychology; Fundamental immunology; IgE; Immunization; Immunoglobulin E - immunology; Immunopathology; Interferon-gamma - immunology; Interleukin-4 - immunology; Interleukin-5 - immunology; Medical sciences; Mice; Mice, Inbred BALB C; mouse; Nose; Respiratory Hypersensitivity - immunology; rhinitis; Rhinitis - immunology; Schistosoma mansoni; Staphylococcus aureus - immunology
• ISSN: 0954-7894; 1365-2222
• DOI: 10.1111/j.1365-2222.2005.02195.x

Summary Background Staphylococcal enterotoxins (SEs) appear to play a role in the pathogenesis of allergic disease. However, little is known whether the nasal exposure to SE affects the development of allergic rhinitis (AR). Objective We sought to determine the in vivo effect of nasal exposure to SE on the development of AR using mouse model. Methods BALB/c mice were intranasally sensitized with Schistosoma mansoni egg antigen (SmEA) in the presence or absence of staphylococcal enterotoxin B (SEB). Control mice were intranasally sensitized with either SEB or SmEA alone. The production of antigen‐specific antibodies including IgE, nasal eosinoplilia and cytokines by nasal mononuclear cells was compared among mice that had or had not received SEB treatment. Results Nasal exposure to SEB enhanced the development of AR in SmEA‐sensitized mice, as manifested by SmEA‐specific IgE production, nasal eosinophilia, and IL‐4 and IL‐5 production by nasal mononuclear cells after Ag challenge. This treatment also elicited IFN‐γ production by SmEA‐primed cells. In addition, these mice produced SEB‐specific IgE whereas mice treated with SEB without SmEA sensitization did not produce SEB‐specific IgE or demonstrate nasal eosinophilia. Conclusion These results suggest that the nasal exposure to SEB enhances susceptibility to AR although the exposure to SE solely does not induce AR.