title: Aggravation of bronchial eosinophilia in mice by nasal and bronchial exposure to Staphylococcus aureus enterotoxin B.
abstract: 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-gamma, IL-12 p40, eotaxin-1 and TGF-beta in bronchi. In addition, nasal SEB elevated concentrations of IL-4, IL-5 and IFN-gamma in serum and bronchial SEB increased titres of OVA-specific and total IgE in serum.
  
  
  CONCLUSIONS
  Our data illustrate the potential of both nasal as well as bronchial SEB to aggravate several features of allergic asthma in a mouse model.
authors.affiliation: Laboratory of Experimental Immunology, Department of Otorhinolaryngology, University Hospitals, Faculty of Medicine, University of Leuven, Belgium. Peter.Hellings@med.kuleuven.be
authors.forename: P W
authors.initials: PW
authors.lastname: Hellings
authors.forename: G
authors.initials: G
authors.lastname: Hens
authors.forename: I
authors.initials: I
authors.lastname: Meyts
authors.forename: D
authors.initials: D
authors.lastname: Bullens
authors.forename: J
authors.initials: J
authors.lastname: Vanoirbeek
authors.forename: P
authors.initials: P
authors.lastname: Gevaert
authors.forename: M
authors.initials: M
authors.lastname: Jorissen
authors.forename: J L
authors.initials: JL
authors.lastname: Ceuppens
authors.forename: C
authors.initials: C
authors.lastname: Bachert
mesh_terms: D000208:Acute Disease; D000818:Animals; D000942:Antigens, Bacterial / Q000494:pharmacology*; D001249:Asthma / Q000276:immunology* / Q000382:microbiology*; D001980:Bronchi / Q000276:immunology* / Q000382:microbiology*; D054413:Chemokine CCL11; D019742:Chemokines, CC / Q000097:blood / Q000235:genetics / Q000276:immunology; D016207:Cytokines / Q000097:blood / Q000235:genetics; D004768:Enterotoxins / Q000494:pharmacology*; D004802:Eosinophilia / Q000276:immunology; D007073:Immunoglobulin E / Q000097:blood; D007371:Interferon-gamma / Q000097:blood / Q000235:genetics / Q000276:immunology; D018664:Interleukin-12 / Q000097:blood / Q000235:genetics / Q000276:immunology; D015847:Interleukin-4 / Q000097:blood / Q000235:genetics / Q000276:immunology; D015848:Interleukin-5 / Q000097:blood / Q000235:genetics / Q000276:immunology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D023421:Models, Animal; D009297:Nasal Mucosa / Q000276:immunology / Q000382:microbiology; D010047:Ovalbumin; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013203:Staphylococcal Infections / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D016212:Transforming Growth Factor beta / Q000097:blood / Q000235:genetics / Q000276:immunology
chemical_list: D000942:Antigens, Bacterial; C515457:Ccl11 protein, mouse; D054413:Chemokine CCL11; D019742:Chemokines, CC; D016207:Cytokines; D004768:Enterotoxins; D015848:Interleukin-5; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta; D018664:Interleukin-12; D015847:Interleukin-4; D007073:Immunoglobulin E; C031818:enterotoxin B, staphylococcal; D007371:Interferon-gamma; D010047:Ovalbumin