Browsing by Subject "food allergy"

Now showing 1 - 6 of 6
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    Epithelial barrier regulation, antigen sampling, and food allergy
    (Elsevier, 2022-09) Cook-Mills, Joan M.; Emmerson, Lauren N.; Microbiology and Immunology, School of Medicine
    Food allergy is often associated with development of atopic dermatitis. Atopic dermatitis is a chronic inflammatory skin condition with a strong association with skin barrier gene mutations. Loss-of-function mutations in skin barrier genes increase transepidermal water loss. Also, reduction of the skin barrier can be mediated by environmental exposures. In preclinical studies of mice with skin barrier disruption, exposure to allergens on the skin induces food allergy. Exposure to food allergens on the skin with coexposure of the skin to other environmental factors induces signals in the skin for activation of food allergy, allergen-specific IgE, and oral food–induced anaphylaxis. In contrast, oral food allergen consumption before skin exposure to food allergen induces tolerance to the food allergen. However, this induction of tolerance may be blocked if skin is exposed to environmental allergens at the time of initial oral food allergen consumption. Further studies are needed to address the mechanisms of induction of food allergy by coexposure of the skin to food allergens, aeroallergens, and other environmental factors. Furthermore, clinical studies are needed to determine the effects of food allergen on skin before skin development of atopic dermatitis.
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    Exposure: Staphylococcus aureus skin colonization predisposes to food allergy in the Learning Early about Allergy to Peanut (LEAP) and LEAP-On studies
    (Elsevier, 2019-08) Cook-Mills, Joan M.; Kaplan, Mark H.; Turner, Matthew J.; Kloepfer, Kirsten M.; Kumar, Rajesh; Pediatrics, School of Medicine
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    Food allergies are a public health crisis we can no longer ignore
    (2017-09-19) Bute, Jennifer J.; Gutierrez, Meghan
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    Management of food allergy in the school setting
    (OceanSide, 2020-09-01) Huddleston, Christina M.; Kloepfer, Kirsten M.; Jin, Jay J.; Vitalpur, Girish V.; Pediatrics, School of Medicine
    Food allergy is a growing health and safety concern that affects up to 8% of school-age children. Because children spend a significant part of their day in school, and the overall number of school-age children with food allergy has been increasing, management of food allergies relies on the collaboration of allergists, families, and schools to treat and prevent acute allergic reactions. For schools, this involves policies centered on food allergen avoidance, preparedness with epinephrine autoinjectors, adequate school personnel training, and accommodations for an equal opportunity learning environment. Partnerships with allergists, primary care providers, students, families, school nurses, and school staff are vital for creating individualized and effective care plans that will allow all children, including those with food allergies, a safe and nurturing learning environment.
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    Mechanism for Initiation of Food Allergy: Dependence on skin barrier mutations and environmental allergen co-stimulation
    (Elsevier, 2018) Walker, Matthew; Green, Jeremy; Ferrie, Ryan; Queener, Ashley; Kaplan, Mark H.; Cook-Mills, Joan M.; Pediatrics, School of Medicine
    Background Mechanisms for the development of food allergy in neonates are unknown but are clearly linked in patient populations to a genetic predisposition towards skin barrier defects. Whether skin barrier defects functionally contribute to development of food allergy is unknown. Objective The purpose of the study was to determine whether skin barrier mutations, that are primarily heterozygous in patient populations, contribute to the development of food allergy. Methods Mice heterozygous for the Flgft and Tmem79ma mutations were skin sensitized with environmental allergens and food allergens. After sensitization, mice received oral challenge with food allergen and then inflammation, inflammatory mediators, and anaphylaxis were measured. Results We define development of inflammation, inflammatory mediators, and food allergen-induced anaphylaxis in neonatal mice with skin barrier mutations following brief concurrent cutaneous exposure to food and environmental allergens. Moreover, neonates of allergic mothers have elevated responses to suboptimal sensitization with food allergens. Importantly, the responses to food allergens by these neonatal mice were dependent on genetic defects in skin barrier function and on exposure to environmental allergens. Blockade of ST2 during skin sensitization inhibited development of anaphylaxis, antigen-specific IgE and inflammatory mediators. The neonatal anaphylactic responses and antigen-specific IgE were also inhibited by oral pre-exposure to food allergen but, interestingly, this was blunted by concurrent pre-exposure of the skin to environmental allergen. Conclusion These studies uncover mechanisms for food allergy sensitization and anaphylaxis in neonatal mice that are consistent with features of human early life exposures and genetics in clinical food allergy and demonstrate that changes in barrier function drive development of anaphylaxis to food allergen.
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    Oral Food Challenge Failures Among Foods Restricted Due to Atopic Dermatitis
    (Elsevier, 2018) Eapen, A. A.; Kloepfer, Kirsten M.; Leickly, Frederick E.; Slaven, James E.; Vitalpur, Girish; Pediatrics, School of Medicine
    BACKGROUND Recent studies have suggested that removing foods from the diet to manage atopic dermatitis (AD), based on positive allergy tests, may lead to immediate allergic reactions on reintroduction of that food. OBJECTIVE The purpose of this study was to examine the frequency of oral food challenge (OFC) failures among foods removed from the diet as suspected AD triggers, focusing on the five major food allergens in the US. METHODS OFCs to egg, milk, peanut, soy, and wheat, performed from 2008-14, at a children's hospital's allergy clinics, were reviewed. OFCs were offered based on history and laboratory values. Reasons for food avoidance were classified as food allergy (IgE-mediated reaction occurring within two hours); sensitization only (lack of introduction due to positive test results); and removal due to test results during AD evaluation. RESULTS There were 442 OFCs performed, with 89 failures (20.1%). Reasons for OFCs included a history of food allergy (320/442; 72.4%); food sensitization without any introduction (77/442; 17.4%); and AD (45/442; 10.2%). OFC failures among those who had food allergy (70/320; 21.9%); sensitization only (13/77; 16.9%); and suspected AD trigger (6/45; 13.3%) did not significantly differ (p=0.63). Wheat was more likely to be avoided than the other four foods for AD concerns (p<0.0001). CONCLUSION The frequency of OFC failure among those who removed foods suspected as AD triggers was 13.3%, indicating a loss of tolerance. Restriction of foods to manage AD must be done with caution and close monitoring.