A study has linked skin sensitization, gastrointestinal inflammation, and food allergy. Using a mouse model, researchers at the Benaroya Research Institute found that skin exposure to a contamination of food antigen and the pro-inflammatory molecule thymic stormal lymphopoietin resulted in food allergy. Adding another protein caused allergic responses in the gut.
This may sound complicated, but what the Benaroya Research colleagues found and published in the Journal of Clinical Investigation is that food allergy may be induced through the skin, providing an early risk model and a possible therapeutic avenue for intervention.
Peanut allergies, for example, are often manifest in children upon their first ingestion of peanuts. This means that having never eaten peanuts before, a child is allergic “pre-exposure.” Since it’s known that food allergies are not from direct exposure via ingestion, they must be from another source. The Benaroya team may have lit on a solution, with skin exposure being an early sensitization trigger.
This sensitivity exposure adds to others which have also been investigated, including exposure through breast milk and in-house contaminants.
The study also opens the avenue of skin exposure as a future treatment avenue or preventative target. If the peanut protein responsible for most allergic reactions in humans is seen as foreign or dangerous by the immune system of the skin, then blocking those immune pathways may prevent the development of peanut allergy.