Airway eosinophilia is not a requirement for allergen-induced airway hyperresponsiveness

Citation
Kg. Tournoy et al., Airway eosinophilia is not a requirement for allergen-induced airway hyperresponsiveness, CLIN EXP AL, 30(1), 2000, pp. 79-85
Citations number
38
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Immunology
Journal title
CLINICAL AND EXPERIMENTAL ALLERGY
ISSN journal
09547894 → ACNP
Volume
30
Issue
1
Year of publication
2000
Pages
79 - 85
Database
ISI
SICI code
0954-7894(200001)30:1<79:AEINAR>2.0.ZU;2-6
Abstract
Background House dust mites (HDMs) are the major source of perennial allerg ens causing human allergic asthma. Animal models mimicking as closely as po ssible the allergic features observed in human asthma are therefore interes ting tools for studying the immunological and pathophysiological mechanisms involved. Especially the role of eosinophils and allergen-specific immunog lobulin (Ig) E in the pathophysiology of airway hyperresponsiveness (AHR) r emains a subject of intense debate. Objective To develop a mouse model of allergic airway inflammation and hype rresponsiveness based on the use of purified house dust mite allergen (Der p 1) as clinical relevant allergen. Furthermore, we studied the effects of low dose allergen exposure on the airway eosinophilia and AHR. Methods On day 0, C57B1/6 mice were immunized with purified Der p 1 intrape ritoneally. From day 14-20, the mice were exposed daily to a 30-min aerosol of different concentrations of house dust mite extract. Results Mice, actively immunized with Der p 1 and subsequently exposed to H DM aerosols, developed AHR, eosinophil infiltration of the airways and alle rgen-specific IgE. Moreover, lowering the concentration of the HDM aerosol also induced AHR and IgE without apparent eosinophil influx into the airway s. Der p 1-sensitized mice exposed to PBS produced IgE, but did not show AH R or eosinophil influx. Conclusion This in vivo model of HDM-induced allergic airway changes sugges ts that AHR is not related to either eosinophil influx or allergen-specific serum IgE, thereby reducing the importance of these factors as essential e lements for allergic AHR.