Early life exposure to a dietary allergen : characteristics, and consequences for allergic sensitisation and disease

The hypothesis of this thesis was that 'the characteristics of early life exposure to dietary egg allergen determine infant atopic phenotype'. Hen egg ovalbumin (OVA) was the dietary allergen investigated. Egg allergy is common in infancy and has implications for later inhalant sensitisation and respiratory allergic disease. Women with a personal or partner history of atopy, were randomised to dietary egg exclusion or a normal healthy diet from 17-20 weeks of pregnancy till the end of breast-feeding. OVA was present in as many blood and breast milk samples of egg avoiding as control women. Atopic women had higher levels of serum OVA than non-atopic women, while atopic and egg avoiding women more often had OVA in breast milk, and in higher quantities, than non-atopic, egg avoiding women. These data suggest that dietary exclusion, particularly by atopic women, does NOT eliminate allergen exposure in early life. Antenatal OVA exposure, in the context of an egg-avoiding and atopic mother, was associated with a greater risk of an atopic phenotype at 6 months of age. Also, exposure via breast milk from an atopic mother suggested a greater risk of later atopy. Maternal serum OVA IgG concentration was shown to mark compliance to an egg exclusion diet and differences in cord concentrations were related to subsequent atopy. These data imply modulatory influences of maternal IgG and atopic environment over developing immune responses and raise the possibility that dietary exclusion as a primary allergy prevention strategy may have adverse consequences. Postnatally, differences in OVA IgG and IgG subclasses were identified for persistently egg sensitised children and elevated OVA IgG1 was associated with later asthma. This suggests that serum OVA IgG1 measurement might be used as an adjunct to skin testing and serum IgE measurement to predict allergic respiratory disease. This work has provided insight into mechanisms that may modulate early life program