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-gamma 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.
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-gamma 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.
Authors: Govindarajan Rajagopalan; Koji Iijima; Manisha Singh; Hirohito Kita; Robin Patel; Chella S David Journal: Infect Immun Date: 2006-02 Impact factor: 3.441