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

Tournoy, Kips, Schou, Pauwels - Clinical & Experimental …, 2000 - Wiley Online Library
Tournoy, Kips, Schou, Pauwels
Clinical & Experimental Allergy, 2000Wiley Online Library
Background House dust mites (HDMs) are the major source of perennial allergens causing
human allergic asthma. Animal models mimicking as closely as possible the allergic
features observed in human asthma are therefore interesting tools for studying the
immunological and pathophysiological mechanisms involved. Especially the role of
eosinophils and allergen‐specific immunoglobulin (Ig) E in the pathophysiology of airway
hyperresponsiveness (AHR) remains a subject of intense debate. Objective To develop a …
Background
House dust mites (HDMs) are the major source of perennial allergens causing human allergic asthma. Animal models mimicking as closely as possible the allergic features observed in human asthma are therefore interesting tools for studying the immunological and pathophysiological mechanisms involved. Especially the role of eosinophils and allergen‐specific immunoglobulin (Ig) E in the pathophysiology of airway hyperresponsiveness (AHR) remains a subject of intense debate.
Objective
To develop a mouse model of allergic airway inflammation and hyperresponsiveness 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, C57Bl/6 mice were immunized with purified Der p 1 intraperitoneally. 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 HDM aerosols, developed AHR, eosinophil infiltration of the airways and allergen‐specific IgE. Moreover, lowering the concentration of the HDM aerosol also induced AHR and IgE without apparent eosinophil influx into the airways. Der p 1‐sensitized mice exposed to PBS produced IgE, but did not show AHR or eosinophil influx.
Conclusion
This in vivo model of HDM‐induced allergic airway changes suggests that AHR is not related to either eosinophil influx or allergen‐specific serum IgE, thereby reducing the importance of these factors as essential elements for allergic AHR.
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