Using mouse models of allergic diseases we have made the novel discovery that allergen challenge to the skin (atopic dermatitis), lung (asthma), or gut (food allergy) elicits not only a local eosinophilic inflammatory response at the site of allergen exposure, but also dysregulates resident eosinophils within the remote (ie allergen non-exposed) lung and gut.

Dysregulation of lung eosinophils primed the airways, causing enhanced susceptibility to an allergic asthma-like response upon inhalation of an unrelated allergen.

These studies are uncovering new mechanisms that may contribute to the “allergic march” in patients.