The clinical cross-reactivity and immunological cross-antigenicity of wheat and barley.

BACKGROUND: Some patients with wheat allergy have been reported to show clinical cross-reactivity to barley. However, it is not clear whether the development of barley allergy in patients with wheat allergy is due to cross-antigenicity between wheat and barley. This study aimed to determine the clinical cross-reactivity and immunological cross-antigenicity of wheat and barley. METHODS: The results of barley oral food challenges (OFCs) were compared before and after oral immunotherapy (OIT) for wheat in nine patients with wheat allergy to estimate the clinical cross-reactivity of wheat and barley. Moreover, we performed enzyme-linked immunosorbent assay (ELISA) inhibition and immunoblotting inhibition using serum from seven patients allergic to wheat and barley. RESULTS: Nine patients who had positive barley-OFC results performed before OIT for wheat were all negative on barley-OFC performed after OIT. In ELISA inhibition, preincubation of serum from patients allergic to wheat and barley with a high barley extract concentration inhibited binding of IgE to wheat extract by less than 10%. On the other hand, wheat and barley extracts equally inhibited binding to barley sIgE at high concentrations. In the immunoblotting inhibition test, the spots of wheat were inhibited but weakly by barley extracts, and most of the spots of barley were inhibited even by low concentrations of the wheat and barley extract. CONCLUSIONS: We showed that barley allergy associated with wheat allergy is caused by cross-reactivity from wheat. The OIT for wheat is one of the promising options for barley allergy.

[COMPARISON OF WHEAL SIZE INDUCED BY BIFURCATED NEEDLE® AND SMARTPRACTICE® PRICK LANCET].

BACKGROUND: There is reportedly a difference in the diameter of the skin reaction induced by different types of skin prick test (SPT) devices. We compared the SPT diagnostic accuracy and wheal size between a Bifurcated Needle® (BN) and SmartPractice® Prick Lancet (PL), which are commercially available in Japan. METHODS: An SPT was performed on 15 adults with and 10 without subjective symptoms of cedar pollinosis who wished to be examined for Japanese cedar pollen (JCP) sensitization. The SPT was performed blindly with a BN or PL with 10mg/ml of histamine dihydrochloride, 50% glycerosaline control, and JCP extract solution (TORII PHARMACEUTICAL CO., LTD., Tokyo, Japan). The wheal sizes induced by the BN and PL were then compared. The JCP-specific IgE antibody titer was measured to compare the sensitivity and specificity of the SPT. RESULTS: Histamine wheal diameters were 6.0 (5.5-6.5) mm by BN and 6.0 (5.5-6.5) mm by PL (p=0.67), and none of the negative control solutions induced wheal. The respective sensitivity and specificity for cedar sensitization were 100% and 86% for BN, 100% and 79% for PL, and the areas under the ROC curve were 0.72 and 0.69 (p=0.32). CONCLUSION: The diagnostic accuracy of cedar pollen extract based on specific IgE-JCP sensitization and the diameter of the wheal produced by a BN and PL were considered equivalent.

Early Discontinuation of Cow's Milk Protein Ingestion Is Associated with the Development of Cow's Milk Allergy.

BACKGROUND: Although early supplementation with cow's milk formula (CMF) reportedly increases the risk of cow's milk allergy (CMA) in breast-fed infants, little is known about the association between the timing of CMF discontinuation and subsequent CMA development. OBJECTIVE: To elucidate the relationship between the timing of CMF discontinuation and CMA development in infants who received CMF in the early days of life. METHODS: Using data from a randomized controlled trial of a birth cohort from 4 Japanese hospitals, we performed a subgroup analysis of participants who ingested CMF in the first 3 days of life. We compared the proportions of participants who developed CMA at age 6 months in those who discontinued CMF ingestion before age 1 month ("DISC <1-month group"), during age 1 to 2 months ("DISC 1-2-month group"), and during age 3 to 5 months ("DISC 3-5-month group") with those who continued CMF ingestion until age 6 months ("continuous group"). The risk ratios (RRs) and 95% CIs for CMA development were calculated. RESULTS: CMA incidence was significantly higher in the DISC <1-month group (n = 7 of 17, 41.2%; RR, 65.7; 95% CI, 14.7-292.5; P < .001), DISC 1-2-month group (n = 3 of 26, 11.5%; RR, 18.4; 95% CI, 3.2-105.3; P = .003), and DISC 3-5-month group (n = 7 of 69, 10.1%; RR, 16.2; 95% CI, 3.4-76.2; P < .001) than in the continuous group (n = 2 of 319, 0.6%). CONCLUSIONS: Early CMF discontinuation, particularly in the first month of life, was associated with CMA development in infants who received CMF in the first 3 days of life.

Food allergy is linked to season of birth, sun exposure, and vitamin D deficiency.

The season of birth and ultraviolet B exposure have been related to the occurrence of food allergy. The levels of vitamin D produced from skin by ultraviolet B exposure might reflect this relationship. Vitamin D is known to induce antimicrobial peptides, protect intestinal flora, enhance the gut epithelial barrier, suppress mast cell activation and IgE synthesis from B cells, and increase the number of tolerogenic dendritic cells and IL-10-producing regulatory T cells. Vitamin D deficiency has been shown to exacerbate sensitization and allergic symptoms in a murine model of food allergy. However, in clinical situations, contradictory observations have been reported regarding the relationship between food allergy and vitamin D deficiency/supplementation. In this review, we have explored the links between food allergy and vitamin D levels. One explanation for the discrepant findings is confounding factors such as race, age, residency, skin color, and epigenetic changes that contribute to vitamin D levels. In addition, the season of birth influences the development of atopic dermatitis, which could lead to food sensitization. Finally, ultraviolet radiation could lead to regulatory T cell expansion and immunosuppression, irrespective of vitamin D status. Based on our current understanding, we believe that correction of vitamin D deficiency by supplementation, appropriate skin care, and sufficient ultraviolet radiation exposure could alter the prognosis of food allergy. To identify potential treatment strategies for food allergy, it is essential to gain a better understanding of the appropriate levels of vitamin D and ultraviolet radiation exposure.