Epicutaneous sensitization to food allergens in atopic dermatitis: What do we know?

Tham, Elizabeth Huiwen; Rajakulendran, Mohana; Lee, Bee Wah; Bever, Hugo P.S. Van

doi:10.1111/pai.13127

Cited by 48 publications

(37 citation statements)

References 129 publications

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“…there is now increasing evidence that early life allergen exposure through the skin causes FA (Figure 2), 21,22 whereas early oral exposure causes tolerance (known as the dual-allergen exposure hypothesis: Figure 3). In the last 5 years, several studies have demonstrated allergen-specific oral tolerance induction to allergenic foods in highrisk children.…”

Section: Pathog Ene S Is Of Food Allergymentioning

confidence: 99%

Epicutaneous sensitization in the development of food allergy: What is the evidence and how can this be prevented?

Brough

Nadeau

Sindher

et al. 2020

Allergy

192

168

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There is increasing evidence regarding the importance of allergic sensitization through the skin. In this review, we provide an overview of the atopic march and immune mechanism underlying the sensitization and effector phase of food allergy. We present experimental models and human data that support the concept of epicutaneous sensitization and how this forms one half of the dual‐allergen exposure hypothesis. We discuss specific important elements in the skin (FLG and other skin barrier gene mutations, Langerhans cells, type 2 innate lymphoid cells, IL‐33, TSLP) that have important roles in the development of allergic responses as well as the body of evidence on environmental allergen exposure and how this can sensitize an individual. Given the link between skin barrier impairment, atopic dermatitis, food allergy, allergic asthma, and allergic rhinitis, it is logical that restoring the skin barrier and prevention or treating atopic dermatitis would have beneficial effects on prevention of related allergic diseases, particularly food allergy. We present the experimental and human studies that have evaluated this approach and discuss various factors which may influence the success of these approaches, such as the type of emollient chosen for the intervention, the role of managing skin inflammation, and differences between primary and secondary prevention of atopic dermatitis to achieve the desired outcome.

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Section: Pathog Ene S Is Of Food Allergymentioning

confidence: 99%

Epicutaneous sensitization in the development of food allergy: What is the evidence and how can this be prevented?

Brough

Nadeau

Sindher

et al. 2020

Allergy

192

168

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“…Epithelial barrier dysfunction of the skin, attributable to a combination of genetic and environmental factors, is not only a hallmark of AD but also a significant risk factor for the development of EC sensitization to food proteins 24 . In our study, a significant increase in the expression of genes encoding innate cytokines (Il6), Th17-type inflammatory cytokine (Il17a), and eosinophil-associated marker (Ccr3) and a decrease in the expression of genes encoding intestinal epithelial tight junction molecule (Cldn4) were observed in the small intestines of EC-challenged mice.…”

Section: Discussionmentioning

confidence: 99%

Small intestinal immune-environmental changes induced by oral tolerance inhibit experimental atopic dermatitis

Baek

Park

et al. 2021

Cell Death Dis

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Atopic dermatitis is a chronic skin inflammatory disease mediated by Th2-type immune responses. Although intestinal immune responses have been shown to play a critical role in the development or prevention of atopic dermatitis, the precise influence of intestinal immunity on atopic dermatitis is incompletely understood. We show here that orally tolerized mice are protected from experimental atopic dermatitis induced by sensitization and epicutaneous (EC) challenge to ovalbumin. Although the expression of Th2-type cytokines in the small intestine of orally tolerized and EC-challenged mice did not change significantly, these mice showed decreased inflammatory responses in the small intestine with restoration of microbial change elicited by the EC challenge. Interestingly, an increase in small intestinal eosinophils was observed with the EC challenge, which was also inhibited by oral tolerance. The role of small intestinal eosinophils and microbiota in the pathogenesis of experimental atopic dermatitis was further substantiated by decreased inflammatory mediators in the small intestine and attenuated Th2-type inflammation in the skin of eosinophil-deficient and microbiota-ablated mice with EC challenges. Based on these data, we propose that the bidirectional interaction between the skin and the intestine has a role in the pathogenesis of atopic dermatitis and that modulation of the intestinal microenvironments could be a therapeutic approach to atopic dermatitis.

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“…The skin microbiome dysbiosis observed in AD skin worsens skin barrier dysfunction, increasing risks of allergen sensitization. [ 47 ] It is also linked with food allergy independent of AD severity. [ 9,48 ] These skin changes are more evident at non‐lesional sites [ 49 ] and show distinctive differences between AD‐associated food allergy and AD non‐food allergy endophenotypes.…”

Section: Introductionmentioning

confidence: 99%

Biotherapeutic Approaches in Atopic Dermatitis

Tham

Koh

Common

et al. 2020

Biotechnology Journal

Self Cite

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The skin microbiome plays a central role in inflammatory skin disorders such as atopic dermatitis (AD). In AD patients, an imbalance between pathogenic Staphylococcus aureus (S. aureus) and resident skin symbionts creates a state of dysbiosis which induces immune dysregulation and impairs skin barrier function. There are now exciting new prospects for microbiome-based interventions for AD prevention. In the hopes of achieving sustained control and management of disease in AD patients, current emerging biotherapeutic strategies aim to harness the skin microbiome associated with health by restoring a more diverse symbiotic skin microbiome, while selectively removing pathogenic S. aureus. Examples of such strategies are demonstrated in skin microbiome transplants, phage-derived anti-S. aureus endolysins, monoclonal antibodies, and quorum sensing (QS) inhibitors. However, further understanding of the skin microbiome and its role in AD pathogenesis is still needed to understand how these biotherapeutics alter the dynamics of the microbiome community; to optimize patient selection, drug delivery, and treatment duration; overcome rapid recolonization upon treatment cessation; and improve efficacy to allow these therapeutic options to eventually reach routine clinical practice.

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Epicutaneous sensitization to food allergens in atopic dermatitis: What do we know?

Cited by 48 publications

References 129 publications

Epicutaneous sensitization in the development of food allergy: What is the evidence and how can this be prevented?

Epicutaneous sensitization in the development of food allergy: What is the evidence and how can this be prevented?

Small intestinal immune-environmental changes induced by oral tolerance inhibit experimental atopic dermatitis

Biotherapeutic Approaches in Atopic Dermatitis

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