Atopic Dermatitis and its Relation to Food Allergy

François Graham; Philippe A. Eigenmann

Disclosures

Curr Opin Allergy Clin Immunol. 2020;20(3):305-310. 

In This Article

Mechanisms of Sensitization to Foods in Patients With Atopic Dermatitis

Atopic dermatitis is characterized by impaired skin barrier and immune dysregulation.[6,25,26] Enhanced absorption of allergen through disrupted skin barrier is thought to lead to a T helper 2 (Th2) response, IgE-class switching, and subsequent clinical food allergy.[27,28] Food allergens penetrating the top layers of the skin (stratum corneum) and exposed to keratinocytes are taken up by local dendritic cells (Langerhans cells), which migrate to local lymph nodes where they induce a Th2 immune response.[29] Moreover, murine studies have shown that innate immune cells (eosinophils and basophils) accumulate in the skin in response to exaggerated thymic stromal lymphopoietin production after cutaneous application of food allergens.[30] Interleukin-4 produced by basophils and eosinophils promotes dendritic cell activation and presentation of food antigens to naïve T cells, which leads to Th2 polarization.[30] and ultimately intestinal IgE-mediated food allergy in mice.[30,31] This is corroborated by the fact that epicutaneously sensitized mice display intestinal mast cell expansion and subsequent anaphylaxis upon exposure to the food allergen.[32]

These in-vivo findings are supported by clinical studies, where epicutaneous sensitization was shown to occur by application of peanut oil on eczematous skin[33] and through environmental exposure to peanuts.[34,35] In addition, exposure to hydrolyzed wheat protein in facial soaps was shown to be a risk factor for a special phenotype of wheat allergy.[36] On the other hand, ingestion of allergens by the oral route generally promotes tolerance.[28]

Genetic factors underlying skin barrier disruption have been associated with increased risk of food allergy. In particular, filaggrin loss-of-function mutation is a risk factor associated with peanut sensitization in children with atopic dermatitis via environmental exposure to house dust peanut protein.[35] Interestingly, filaggrin mutation was shown to be a risk factor for peanut allergy but not for other food allergens in preschool children.[37] Furthermore, missense mutations in serine peptidase inhibitor Kazal type 5 (SPINK5) have been associated with food challenge-proven food allergy.[38]

Skin microbiome dysbiosis also plays a role in predisposing food sensitization in patients with atopic dermatitis by contributing to skin barrier dysfunction.[28] Staphylococcal superantigens (such as Staphylococcal enterotoxin B) were shown to enhance peanut epicutaneous sensitization in mice.[39] In addition, higher rates of food allergy were found in children with atopic dermatitis colonized with Staphylococcus aureus.[40]

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