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Aggravation of bronchial eosinophilia in mice by nasal and bronchial exposure to Staphylococcus aureus enterotoxin B
Author(s) -
Hellings P. W.,
Hens G.,
Meyts I.,
Bullens D.,
Vanoirbeek J.,
Gevaert P.,
Jorissen M.,
Ceuppens J. L.,
Bachert C.
Publication year - 2006
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/j.1365-2222.2006.02527.x
Subject(s) - medicine , immunology , eotaxin , ovalbumin , asthma , immunoglobulin e , eosinophilia , enterotoxin , staphylococcus aureus , allergic inflammation , allergy , inflammation , eosinophil , antigen , antibody , biology , genetics , escherichia coli , bacteria , gene , biochemistry
Summary Background The role of bacterial enterotoxins like Staphylococcus aureus enterotoxin B (SEB) in allergic asthma remains unknown. We used a mouse model of airway allergy to study the effects of nasal or bronchial contact with SEB on bronchial allergic inflammation. Methods The features of allergic asthma were induced in ovalbumin (OVA)‐sensitized mice (days 1–13) by repeated exposures to nebulized OVA (days 33–37). Nasal or bronchial application of SEB was performed on three occasions (days 33–35–37), and the effects on bronchial inflammation, IgE titres and expression levels of mRNA for T helper type 2 cytokines and other inflammatory mediators were evaluated. Results Both nasal and bronchial SEB enhanced the allergen‐induced bronchial inflammation, as reflected by more eosinophilic inflammation in the airway lumen and in bronchial tissue. Aggravation of experimental asthma correlated with higher expression of mRNA for IL‐5, IL‐4, IFN‐γ, IL‐12 p40, eotaxin‐1 and TGF‐β in bronchi. In addition, nasal SEB elevated concentrations of IL‐4, IL‐5 and IFN‐γ in serum and bronchial SEB increased titres of OVA‐specific and total IgE in serum. Conclusion Our data illustrate the potential of both nasal as well as bronchial SEB to aggravate several features of allergic asthma in a mouse model.