Mark S. Wilson. Molecular Immunology Division. National Instiutes for Medical Research, MRC. Mill Hill. London. UK.
The sequential progression of allergic symptoms from atopic eczema, food allergy, rhinitis and asthma have been widely reported and referred to as ‘The Atopic March’. Co-morbidities of allergic conditions and the over-dispersed distribution of allergic diseases within few individuals have also been identified. These data suggest that allergic diseases may be linked; however the relationships between allergic symptoms are unclear. To separate cause from consequence, we are investigating the immunological interactions between these disease phenotypes and have developed experimental models of allergic asthma, allergic rhinitis and food allergy. These models are used to ask whether food allergy, and/or upper airway rhinitis influence the development of lower airway asthma. Mice sensitized and orally challenged with crude peanut antigen (CPA) are subsequently sensitized and challenged, in the lower airways, with house dust mite (HDM). A cohort of peanut-allergic mice will also be sensitized and challenged in the upper airways with ragweed (RW) prior to lower airway HDM challenge. We hypothesize that peanut allergy and RW-induced rhinitis will exacerbate HDM-sensitization (IgE) and HDM-induced airway inflammation. The molecular mechanisms of such interactions will be investigated and tested. Our studies and latest observations will be presented. This work is supported by the Medical Research Council (MRC), UK.