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Childhood food allergy has been linked to environmental and genetic factors that must coexist to trigger allergy. The factors contributing to food allergy include the genetics that change skin absorbency, use of infant cleansing wipes that leave soap on the skin, skin exposure to allergens in dust and skin exposure to food from those providing infant care. Food allergy is triggered when these factors occur together.
According to the study author, Joan Cook-Mills, a professor of allergy-immunology at Northwestern University Feinberg School of Medicine, food allergies are on the rise, the prevalence of reported food allergy increased 18 percent among children under age 18 years from 1997 to 2007. Recent data also show hospitalizations with diagnoses related to food allergies have increased among children.
Reducing baby’s skin exposure to the food allergens by washing of hands before handling and limiting the use of infant wipes that leave soap on the skin can reduce the allergy. Clinical evidence shows up to 35 percent of children with food allergies have atopic dermatitis and much of that is explained by at least three different gene mutations that reduce the skin barrier.
Researchers used a neonatal mouse model with skin barrier mutations and tried exposing its skin to food allergens like peanuts. The peanuts alone had no effect, handling baby with contaminated hands to environmental allergens in dust in a home may be the cause. The outer skin layer is made of lipids (fats), and the soap in the wipes disrupts that barrier. Skin problems that occur with skin barrier mutations may not be visible until long after a food allergy started.
The neonatal mice with the mutations had normal-appearing skin, and the dry itchy skin of dermatitis did not develop until the mice were a few months old, the equivalent of a young adult in human years. After the neonatal mice received three to four skin exposures of food and dust allergens for 40 minutes during a two-week period, they were given egg or peanut by mouth. The mice had allergic reactions at the site of skin exposure, allergic reactions in the intestine, and the severe allergic food reaction of anaphylaxis that is measured by decreased body temperature.
A skin barrier dysfunction was necessary for food allergy to develop in the mice, but there is severe to mild skin dysfunction with eczema or atopic dermatitis, which in its mildest form may appear to be dry skin. In patients with skin-barrier defects, there are changes in the proteins in the skin as a result of mutations in the genes. These gene mutations in patients are primarily heterozygous, which means there is a mutation in one of the two copies of a gene.
Neonatal mice were also heterozygous for skin barrier mutations. The mice were co-exposed to food allergens such as egg and peanut proteins, allergens in dust (house dust mite or Alternaria alternata mold) and sodium lauryl sulfate, a soap present in infant cleansing wipes. These novel animal studies provide a basis to test interventions that will effectively block the development of food allergy in infants and children.
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