Peanut allergens are rapidly transferred in human breast milk and can prevent sensitization in mice

Bernard, Hervé; Ah‐Leung, S.; Drumare, Marie-Françoise; Féraudet-Tarisse, Cécile; Verhasselt, Valérie; Wal, Jean‐Michel; Créminon, Christophe; Adel‐Patient, Karine

doi:10.1111/all.12411

Cited by 88 publications

(88 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Likewise, it has been described that the recovery of peanut allergens is strongly influenced by the matrix. Apart from our own study investigation on the passage of Ara h 2 into breast milk [19], to our knowledge there is only the French study on 2 lactating mothers that detected Ara h 6 concentrations in the pg/mL range [18]. However, to the best of our knowledge, we are the first group to study the ability of 2 single, clinically relevant peanut allergens to pass into human breast milk.…”

Section: Discussionmentioning

confidence: 99%

“…In terms of Ara h 6, Bernard et al [18] could show that Ara h 6 is excreted as free allergen and IgG-Ara h 6 and IgA-Ara h 6 immune complexes into breast milk after consuming 30 g of roasted peanuts. However, the concentrations of either free or complexed Ara h 6 in the pg/mL range up to 3.4 ng/mL come close to the concentrations we measured in our study group.…”

Section: Discussionmentioning

confidence: 99%

“…Vadas et al [17] presented preliminary data on 23 healthy, lactating women in Canada and showed that whole peanut protein extract was detected in 11 of 23 subjects (48%) at a concentration ranging from 120 to 430 ng/mL within 1-3 h. Bernard et al [18] investigated Ara h 6 in samples of 2 lactating women shortly after peanut consumption, with concentrations in the picogram/milliliter (pg/mL) range but long-lasting excretion up to 26 h after peanut ingestion. To the best of our knowledge, we have recruited the largest study population of lactating women in Germany since 2004 that has been assessed prospectively ( n = 40) for the transfer of peanut proteins into breast milk after consuming 100 g of dry roasted peanuts after an otherwise legume-free diet.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Detection of the Peanut Allergens Ara h 2 and Ara h 6 in Human Breast Milk: Development of 2 Sensitive and Specific Sandwich ELISA Assays

Schocker

Scharf

Kull

et al. 2017

Int Arch Allergy Immunol

View full text Add to dashboard Cite

Background: Little is known about breast milk as a vehicle for tolerance development or sensitization to peanuts very early in life. Thus, well-characterized and highly sensitive detection systems for the reliable determination of peanut allergens in breast milk are mandatory. Methods: For the quantification of the marker allergens Ara h 2 and Ara h 6 in the low nanogram per milliliter range in breast milk samples of a German cohort, sensitive and highly specific sandwich ELISAs were optimized and validated. Results: The Ara h 2 ELISA revealed a limit of detection (LOD) of 1.3 ng Ara h 2/mL and a quantification range of 2.3-250 ng/mL, the Ara h 6 ELISA showed an LOD of 0.7 ng/mL and a working range of 1.1-14.4 ng/mL. The assays showed no relevant cross-reactivity against other potentially cross-reactive legume, seed, and tree nut extracts (<0.01%, except for Ara h 1 in the Ara h 2 ELISA <0.1%). Ara h 2 was detectable in breast milk samples from 14/40 (35%) of the participants in concentrations from 2.3 to 184 ng/mL, Ara h 6 appeared in 9/40 (22.5%) of the lactating mothers between 1.1 and 9.7 ng/mL, and 1 highly positive sample with 79 ng/mL. Both allergens appeared at the same time points, but Ara h 6 in lower concentrations than Ara h 2. Conclusions: Sensitive and specific diagnostic tools for the determination of Ara h 2 and Ara h 6 in human breast milk were established. The kinetics of secreted Ara h 2 and Ara h 6 seem to be similar but with a difference in concentration. Follow-up investigations on their tolerogenic or sensitizing properties in breast milk become now accessible.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Detection of the Peanut Allergens Ara h 2 and Ara h 6 in Human Breast Milk: Development of 2 Sensitive and Specific Sandwich ELISA Assays

Schocker

Scharf

Kull

et al. 2017

Int Arch Allergy Immunol

View full text Add to dashboard Cite

show abstract

“…They received a specific diet; using specific monoclonal antibodies and immunoassays developed in the laboratory, Ara h 1 was not detected (data not shown) [20,21]. The Ara h 6 level in the diet was <5 ppm, determined with specific immunoassays developed in the laboratory [22]. All animal experiments were performed according to European Community Rules of Animal Care with authorization No.…”

Section: Methodsmentioning

confidence: 99%

Cutaneous or Respiratory Exposures to Peanut Allergens in Mice and Their Impacts on Subsequent Oral Exposure

Wavrin

Bernard

Wal

et al. 2014

Int Arch Allergy Immunol

View full text Add to dashboard Cite

Background: Recent data suggested that non-gastrointestinal exposure can lead to sensitisation to food allergens. We thus assessed the immune impact of respiratory or cutaneous exposure to peanut proteins on non-altered epithelium and investigated the effect of such pre-exposure on subsequent oral administration of peanut. Methods: BALB/cJmice were exposed to purified Ara h 1 or to a non-defatted roasted peanut extract (PE) by simple deposit of allergens solutions on non-altered skin or in the nostrils. Exposures were performed 6 times at weekly intervals. Pre-exposed mice then received intra-gastric administrations of PE alone or in the presence of the Th2 mucosal adjuvant cholera toxin (CT). The specific humoral and cellular immune response was assessed throughout the protocol. Results: Bothcutaneous and respiratory exposures led to the production of specific IgG1. Local and systemic IL-5 and IL-13 production were also evidenced, demonstrating activation of specific Th2 cells. This effect was dose-dependent and most efficient via the respiratory route. Moreover, these pre-exposures led to the production of specific IgE antibodies after gavage with PE, whatever the presence of CT. Conclusions: Cutaneous or respiratory exposures to peanut induce Th2 priming in mice. Moreover, pre-exposures promote further sensitisation via the oral route without the use of CT; this proposes a new adjuvant-free experimental model of sensitisation to food that may reflect a realistic exposure pattern in infants. These results also suggest that non-gastrointestinal peanut exposure should be minimised in high-risk infants, even those with non-altered skin, to potentially reduce allergic sensitisation to this major food allergen.

show abstract

“…In a mouse model, mice exposed to nanograms of egg ovalbumin antigen through breast milk were protected from ovalbumin-induced allergic airway disease and TGF-β from breast milk was critical for tolerance induction, suggesting that variability in breast milk allergen content, TGF-β, and allergen-specific immunoglobulin may contribute to heterogeneity of results on allergy prevention by breastfeeding. Presence of peanut in maternal diet was associated with a reduced risk of food allergy in the offspring in both humans and mice [41,45,57] . Collectively, there is currently no conclusive evidence that breastfeeding protects from development of food allergy, potentially reflecting the environmental factors that affect the composition of maternal milk.…”

Section: Breastfeedingmentioning

confidence: 99%

Mechanisms of Tolerance Induction

Nowak‐Węgrzyn¹,

Chatchatee²

2017

Ann Nutr Metab

View full text Add to dashboard Cite

Food allergy results from failure in oral tolerance that usually occurs in infancy or early childhood. Exposure to peanut and hen's egg via the inflamed and disrupted epithelial barrier in children with severe atopic dermatitis is a risk factor for the development of allergy to these foods and supports the hypothesis that epicutaneous exposure in the absence of oral feeding is an important pathway of allergic IgE sensitization in infants. In recent years, the collective evidence has pointed toward the protective effect of an early feeding with peanut and egg in children with eczema, taking advantage of the pathways underlying oral tolerance to counteract epicutaneous exposure. An addendum to the NIAID food allergy guidelines recommends introduction of peanut into the diet of 4- to 6-month-old infants with severe eczema or egg allergy as an effective strategy to prevent peanut allergy. Strategies aimed at restoring the skin barrier are currently explored as an alternative approach of prevention of eczema and allergic sensitization. Manipulation of the diet via supplementation with probiotics and prebiotics to restore the healthy gut microbiota represents another potential pathway to induction of tolerance in the gut. Oral, epicutaneous, and sublingual routes of food immunotherapy are promising and induce desensitization in the majority of the treated subjects with food allergy but are not proven to restore permanent oral tolerance. Rigorous multicenter randomized clinical trials are necessary to elucidate the optimal timing, dose, duration, as well as the preventive and therapeutic effects of these diverse approaches.

show abstract

Peanut allergens are rapidly transferred in human breast milk and can prevent sensitization in mice

Abstract: The low quantities of immunologically active allergens transferred through breast milk may prevent instead of priming allergic sensitization to peanut.

Cited by 88 publications

References 55 publications

Detection of the Peanut Allergens Ara h 2 and Ara h 6 in Human Breast Milk: Development of 2 Sensitive and Specific Sandwich ELISA Assays

Detection of the Peanut Allergens Ara h 2 and Ara h 6 in Human Breast Milk: Development of 2 Sensitive and Specific Sandwich ELISA Assays

Cutaneous or Respiratory Exposures to Peanut Allergens in Mice and Their Impacts on Subsequent Oral Exposure

Mechanisms of Tolerance Induction

Contact Info

Product

Resources

About