A team of researchers from several institutes in France used technology developed by Austin-based company Luminex Corporation to analyze the interaction between the skin, gut and lungs in allergic reactions. The study was published in the journal Respiratory Research and is entitled “Food allergy enhances allergic asthma in mice.”
Atopic march corresponds to the progression of atopic disorders of the skin, such as atopic dermatitis (also known as eczema) or in the gut (related to intestinal inflammation) such as food allergies in infants, which leads to sensitization to aeroallergens, resulting in allergic rhinitis and bronchial asthma in older children and adults. The relationship between skin, gut and pulmonary inflammation in atopic march is poorly understood.
It has been previously suggested that food allergy in childhood can increase Th2 inflammation (antibody-mediated immune response against parasites, bacteria, allergens and toxins) exacerbating asthma, indicating a link between food allergy and allergic asthma.
One common food allergen is found in eggs – ovalbumin (OVA) — and it can cause anaphylaxis (a severe, potentially life-threatening allergic reaction) and atopic dermatitis in infants. House dust mites (HDM) are also strongly associated with atopic dermatitis, considered its main allergen. Together, OVA and HDM play a central role in atopic march by inducing food allergy, skin sensitization and asthma.
In this study, an allergic mouse model of the American HDM Dermatophagoides farinae (Der-f)-induced asthma with primary OVA-induced food allergy was established to mimic the atopic march events and provide insight into the impact of food allergies on asthma.
Mice were sensitized for food allergy to OVA (by intra-peritoneal sensitization and intra-gastric challenge), respiratory allergy to HDM (by percutaneous sensitization and intra-nasal challenges with Der-f or both. Digestive, systemic and respiratory factors were assessed, and immune response elements were quantified by Luminex.
Researchers observed that OVA-mediated gut allergy increased intestinal permeability, while Der f-induced respiratory allergy resulted in lung inflammation. In dual allergy mice, Der f-induced asthma was found to be worse, with stronger airway hyperresponsiveness (AHR) and inflammation response with pulmonary cell infiltration (especially with eosinophils – white blood cells associated to mechanisms controlling allergy and asthma).
In the presence of both allergies, antibody levels of IgG1 (which protects the body from infections) and IgE (associated to allergic diseases) were significantly higher. Both AHR and lung inflammation increased upon a second pulmonary challenge. Gut sensitization to OVA was therefore found to result in an amplification of the Der f-induced asthma in mice.
The results revealed the importance of the synergy between gut, skin and lungs and their respective immune responses in the development of asthma. Food sensitization to one allergen primes the immune system to develop an enhanced pulmonary inflammation linked to an immune over-reaction in response to a different, unrelated allergen. Future studies with this allergic mouse model can further elucidate the mechanisms of atopic march.