Estimating the Risk of Severe Peanut Allergy Using Clinical Background and IgE Sensitization Profiles

Background: It is not well-understood why symptom severity varies between patients with peanut allergy (PA).Objective: To gain insight into the clinical profile of subjects with mild-to-moderate and severe PA, and investigate individual and collective predictive accuracy of clinical background and IgE to peanut extract and components for PA severity.Methods: Data on demographics, patient history and sensitization at extract and component level of 393 patients with probable PA (symptoms ≤ 2 h + IgE sensitization) from 12 EuroPrevall centers were analyzed. Univariable and penalized multivariable regression analyses were used to evaluate risk factors and biomarkers for severity.Results: Female sex, age at onset of PA, symptoms elicited by skin contact with peanut, family atopy, atopic dermatitis, house dust mite and latex allergy were independently associated with severe PA; birch pollen allergy with mild-to-moderate PA. The cross-validated AUC of all clinical background determinants combined (0.74) was significantly larger than the AUC of tests for sensitization to extract (0.63) or peanut components (0.54–0.64). Although larger skin prick test wheal size, and higher IgE to peanut extract, Ara h 1 and Ara h 2/6, were associated with severe PA, and higher IgE to Ara h 8 with mild-to-moderate PA, addition of these measurements of sensitization to the clinical background model did not significantly improve the AUC.Conclusions: Models combining clinical characteristics and IgE sensitization patterns can help establish the risk of severe reactions for peanut allergic patients, but clinical background determinants are most valuable for predicting severity of probable PA in an individual patient.

Food Allergy Adjuvant and Early Immune Effects of Oral Exposure to Known and Suspected Gut Barrier Disruptors

Background: Exposure to adjuvants with a food allergen has been shown to promote sensitization and development of food allergy in animal models. Barrier disrupting capacities have been suggested to be one mechanism of adjuvant action. In this study, we investigated how gut barrier disrupting compounds affected food allergy development in a mouse model of peanut allergy. Sensitization and clinical peanut allergy in C3H/HEOuJ mice were assessed after repeated oral exposure to peanut extract together with cholera toxin (CT), the mycotoxin deoxynivalenol (DON), house dust mite (HDM) or the pesticide glyphosate (GLY). In addition, we investigated early effects 4 to 48 hours after a single exposure to the compounds, by assessing markers of intestinal barrier permeability, alarmin production, intestinal epithelial responses, and local immune responses.Results: CT and DON exerted adjuvant effects on peanut allergy development assessed as clinical anaphylaxis in mice. The early markers were consistently only affected by DON, observed as increased IL-33 (interleukin 33) and thymic stromal lymphopoietin (TSLP) alarmin production in intestines and Interleukin 33 receptor ST2 in serum. DON also induced an inflammatory immune response in lymph node cells stimulated with lipopolysaccharide (LPS). HDM and GLY did not promote clinical food allergy and affected few (or none) of the early markers at the present doses.Conclusions: Oral exposure to CT and DON promoted development of clinical anaphylaxis in the peanut allergy mouse model. DON, but not CT, affected the early markers measured in the present study, indicating that DON and CT have different modes of action at the early stages of peanut sensitization.

A case report of mono-sensitization to peanut component Ara h6

Peanut is the most common food allergen in the US, affecting 1-2 % of the population and studies show that it is still on the rise. Component testing has offered better insight into the likelihood of reactivity with exposure. Extensive literature shows Arachis hypogea (Ara h) 2 as being the most clinically significant component identified to correlate with reactivity with exposure to the peanut protein, however there is minimal research on the reactivity of Ara h6. This case report describes a patient with a clinical reaction to peanut as a toddler and subsequent positivity on annual skin testing with commercial peanut extract, likely confounded by positive birch with advancing age. Immuno CAP testing revealed a negative Ara h2 and positive Ara h6, describing mono-sensitization to Ara h 6 and high probability of clinical reactivity. The importance of this case is to raise awareness of other highly allergenic components in patients with peanut allergy.

Isolation of Aflatoxin B1 from Moldy Foods by Solid-Phase Extraction Combined with Bifunctional Ionic Liquid-Based Silicas

A solid-phase extraction method was developed by using new bifunctional ionic liquid-based silicas as sorbents to isolate aflatoxin B1 from moldy corn and peanut. Firstly, according to the adsorption efficiency, two sorbents imidazolium chloride-butylimidazolium chloride-based silica (Sil@BIm-Im) and imidazolium chloride-hexylimidazolium chloride-based silica (Sil@HIm-Im) were selected. The RSM was introduced to optimize adsorption conditions such as methanol/water ratio, time, and pH. Sil@HIm-Im, which had the highest adsorption efficiency, was used in SPE as a sorbent. After 2.0 mL of loading samples, washing solvents were optimized as 6.0 mL and 4.0 mL of water for corn and peanut, 2.0 mL of acetonitrile, and 3.0 mL of methanol. 3.0 mL of methanol/acetic acid (2.0% vol.) was investigated as an elution solvent. Finally, 0.009 μg/g and 0.023 μg/g of aflatoxin B1 were obtained in corn and peanut extract with recoveries of 80.0%–103.3% and RSDs of 2.37%–6.58%.