Predictors and biomarkers of food allergy and sensitization in early childhood

Davis, E. G.; Jackson, Courtney M.; Ting, Tiffany; Harizaj, Albana; Järvinen, Kirsi M.

doi:10.1016/j.anai.2022.04.025

Cited by 14 publications

(26 citation statements)

References 74 publications

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“…FA generally coexists with AD in children, and it is the most frequent cause of outpatient anaphylaxis ( 18 ). Other features of food allergy include abdominal pain, flatulence, vomiting, and diarrhea ( 19 ). Eosinophilic esophagitis (EoE) characterized by the chronic eosinophilic inflammation is closely correlated with food allergy ( 20 ).…”

Section: The Atopic Marchmentioning

confidence: 99%

Claudin-1 Mediated Tight Junction Dysfunction as a Contributor to Atopic March

Xia

Cao²,

Zheng³

2022

Front. Immunol.

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Atopic march refers to the phenomenon wherein the occurrence of asthma and food allergy tends to increase after atopic dermatitis. The mechanism underlying the progression of allergic inflammation from the skin to gastrointestinal (GI) tract and airways has still remained elusive. Impaired skin barrier was proposed as a risk factor for allergic sensitization. Claudin-1 protein forms tight junctions and is highly expressed in the epithelium of the skin, airways, and GI tract, thus, the downregulation of claudin-1 expression level caused by CLDN-1 gene polymorphism can mediate common dysregulation of epithelial barrier function in these organs, potentially leading to allergic sensitization at various sites. Importantly, in patients with atopic dermatitis, asthma, and food allergy, claudin-1 expression level was significantly downregulated in the skin, bronchial and intestinal epithelium, respectively. Knockdown of claudin-1 expression level in mouse models of atopic dermatitis and allergic asthma exacerbated allergic inflammation, proving that downregulation of claudin-1 expression level contributes to the pathogenesis of allergic diseases. Therefore, we hypothesized that the tight junction dysfunction mediated by downregulation of claudin-1 expression level contributes to atopic march. Further validation with clinical data from patients with atopic march or mouse models of atopic march is needed. If this hypothesis can be fully confirmed, impaired claudin-1 expression level may be a risk factor and likely a diagnostic marker for atopic march. Claudin-1 may serve as a valuable target to slowdown or block the progression of atopic march.

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Section: The Atopic Marchmentioning

confidence: 99%

Claudin-1 Mediated Tight Junction Dysfunction as a Contributor to Atopic March

Xia

Cao²,

Zheng³

2022

Front. Immunol.

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“…Food allergies are thought to arise due to a combination of genetic and environmental factors [ 14 , 15 ]. Genetic association studies have identified some risk alleles for food allergies, particularly in the genes MALT1 , FLG , and HLA ; these findings implicate genes involved in immune and barrier function in the development of food allergies [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Microbiome Therapeutics for Food Allergy

2022

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The prevalence of food allergies continues to rise, and with limited existing therapeutic options there is a growing need for new and innovative treatments. Food allergies are, in a large part, related to environmental influences on immune tolerance in early life, and represent a significant therapeutic challenge. An expanding body of evidence on molecular mechanisms in murine models and microbiome associations in humans have highlighted the critical role of gut dysbiosis in the pathogenesis of food allergies. As such, the gut microbiome is a rational target for novel strategies aimed at preventing and treating food allergies, and new methods of modifying the gastrointestinal microbiome to combat immune dysregulation represent promising avenues for translation to future clinical practice. In this review, we discuss the intersection between the gut microbiome and the development of food allergies, with particular focus on microbiome therapeutic strategies. These emerging microbiome approaches to food allergies are subject to continued investigation and include dietary interventions, pre- and probiotics, microbiota metabolism-based interventions, and targeted live biotherapeutics. This exciting frontier may reveal disease-modifying food allergy treatments, and deserves careful study through ongoing clinical trials.

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“…Four articles in this issue explore this concept through different ideas. [1][2][3][4] It is important to remember that prevention can occur at 2 levels: (1) primary: preventing the disease from occurring; or (2) secondary: preventing the progression or worsening of disease (often called disease-modifying). In terms of allergy, the blocking of the atopic march of atopic dermatitis to other atopic diseases (asthma, food allergy, or allergic rhinitis) is secondary prevention, 5,6 whereas preventing food allergy by early introduction of foods is primary prevention.…”

mentioning

confidence: 99%

“…One successful strategy for the prevention of food allergy is the use of early introduction of foods in high-risk populations of egg allergy and patients with moderate to severe atopic dermatitis, which was originally pioneered by Du Toit et al 8 In the review by Davis et al, 1 the risks of food allergy and sensitization are evaluated. They noted that the rapid rise in food allergy and sensitization in the past 20 years cannot be owing to simple genetics, despite the known heritable risks for food allergy.…”

mentioning

confidence: 99%

“…Interestingly, the studies suggest that a lack of diversity in the gut microbiome with more immature species may favor the development of food allergy. 1 They suggest that additional studies are needed to evaluate metabolomics to resolve conflicting data. Consistent with the concepts of Platts-Mills, 4 the rise and prevention of atopic disease is not as simple as the hygiene hypothesis and genetics but a more complex interplay of multiple pathways.…”

mentioning

confidence: 99%

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