Partially Hydrolysed Whey-Based Infant Formula Improves Skin Barrier Function.

Sébastien Holvoet,Hans-Uwe Simon,Dagmar Simon,Lénaïck Dupuis,Carine Blanchard,Ryan S Carvalho,Tristan Bourdeau,Betsy Hughes-Formella,Dominique Donnicola,Sibylle Koletzko,Sophie Nutten,Jonathan M Spergel

doi:10.3390/nu13093113

Abstract

Specific partially hydrolysed whey-based infant formulas (pHF-W) have been shown to decrease the risk of atopic dermatitis (AD) in infants. Historically, AD has been associated primarily with milk allergy; however, defective skin barrier function can be a primary cause of AD. We aimed to ascertain whether oral supplementation with pHF-W can improve skin barrier function. The effect of pHF-W was assessed on transepidermal water loss (TEWL) and antibody productions in mice epicutaneously exposed to Aspergillus fumigatus. Human primary keratinocytes were stimulated in vitro, and the expression of genes related to skin barrier function was measured. Supplementation with pHF-W in neonatal mice led to a significant decrease in TEWL and total IgE, but not in allergen-specific antibody levels. The whey hydrolysate was sufficient to decrease both TEWL and total IgE. Aquaporin-3 gene expression, linked with skin hydration, was modulated in the skin of mice and human primary keratinocytes following protein hydrolysate exposure. Skin barrier improvement may be an additional mechanism by which pHF-W may potentially reduce the risk of AD development in infants. Further human studies are warranted to confirm the clinical efficacy of these observations.

Highlights

IntroductionRecent evidence in murine studies has demonstrated that allergen application (including ovalbumin, peanut, milk protein, or Aspergillus fumigatus) on an impaired barrier can lead to systemic sensitisation [16,17,18,19,20]
Additional studies have demonstrated that increased transepidermal water loss (TEWL) in the first weeks of life was associated with an increased risk of atopic dermatitis (AD) development, which was independent of family history [14], yet the retraction of a key publication added controversy to the field [15]
AD is recognised as a major risk factor for the development of food allergy [22], and as a consequence, preventive strategies for food allergy may require a primary prevention of AD or skin barrier impairment [23]

Summary

Introduction

Recent evidence in murine studies has demonstrated that allergen application (including ovalbumin, peanut, milk protein, or Aspergillus fumigatus) on an impaired barrier can lead to systemic sensitisation [16,17,18,19,20]. These studies, along with genetic studies linking filaggrin mutations with food allergy [21], have led to the hypothesis that allergic sensitisation may be secondary to AD or skin barrier impairment. AD is recognised as a major risk factor for the development of food allergy [22], and as a consequence, preventive strategies for food allergy may require a primary prevention of AD or skin barrier impairment [23]

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Conclusion