Figure 2. Mechanisms of skin barrier dysfunction in atopic
dermatitis resulting in food allergy.
Environmental pollutants, detergents, microbial dysbiosis and genetics
such as FLG loss of function mutations can lead to disruptions to
the epithelial barrier. Skin barrier impairment leads to skin
inflammation resulting in atopic dermatitis. Epicutaneous exposure to
food allergens in the context of an impaired barrier may trigger food
allergen sensitization through Th2-dependent pathways: Specific resident
dendritic cell (DC) subsets capture allergens in the skin and transport
them to skin-draining lymph nodes where they are presented to CLA+ skin
homing T cells. IL‐4 and IL‐13 cytokines promote B‐cell isotype
switching to specific IgE (sIgE), and upon differentiating into plasma
cells, yield allergen‐specific IgE antibodies. The sIgE bind to
high‐affinity FcεRI receptors on the surface of mast cells and
basophils. During the sensitization process, a memory pool of
allergen‐specific B cells and T helper 2 cells are produced. Upon
subsequent oral antigen exposure (consumption of the allergenic food),
cross-linking of sIgE on the FcεRI receptors trigger mast cell
degranulation, release of histamine and other inflammatory mediators,
culminating in the clinical allergic response. The presence of S.
aureus enhances pro-inflammatory responses which heighten risk of food
allergy development. S. aureus colonization, such as bymethicillin-resistant S. aureus (MRSA), and exposure to
staphylococcal enterotoxin B (SEB), has been shown to increase risk of
food allergy (FA) independent of AD severity. S. aureus abundance
was also found to be positively correlated with transepidermal water
loss (TEWL) in patients with AD and FA. (Created with BioRender.com)