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Polymorphisms affecting vitamin D–binding protein modify the relationship between serum vitamin D (25[OH]D3) and food allergy - 05/02/16

Doi : 10.1016/j.jaci.2015.05.051 
Jennifer J. Koplin, PhD a, b, Noor H.A. Suaini, BSc (Hons) a, d, Peter Vuillermin, MBBS, FRACP, PhD a, c, Justine A. Ellis, PhD a, d, Mary Panjari, PhD a, Anne-Louise Ponsonby, MBBS, FAFPHM, PhD a, d, Rachel L. Peters, MPH a, d, Melanie C. Matheson, PhD a, b, David Martino, PhD a, d, Thanh Dang, PhD a, Nicholas J. Osborne, PhD e, , Pamela Martin, PhD a, Adrian Lowe, PhD a, b, Lyle C. Gurrin, PhD a, b, Mimi L.K. Tang, MD, PhD a, d, f, Melissa Wake, MD, FRACP a, d, g, Terry Dwyer, PhD a, , John Hopper, PhD b, Shyamali C. Dharmage, MBBS, MSc, MD, PhD a, b, Katrina J. Allen, MBBS, BMedSc, FRACP, PhD a, d, f, h,
for the

HealthNuts Study

a Murdoch Childrens Research Institute, Parkville, Australia 
b School of Population and Global Health, University of Melbourne, Parkville, Australia 
c Child Health Research Unit, Barwon Health and Deakin University, Geelong, Australia 
d Department of Paediatrics, University of Melbourne, Parkville, Australia 
e European Centre for Environment and Human Health, University of Exeter Medical School, Cornwall, United Kingdom 
f Department of Allergy and Immunology, Royal Children's Hospital, Parkville, Australia 
g Centre for Community Child Health, Royal Children's Hospital, Parkville, Australia 
h School of Inflammation and Repair, University of Manchester, Manchester, United Kingdom 

Corresponding author: Katrina J. Allen, MBBS, BMedSc, FRACP, PhD, Murdoch Childrens Research Institute, Royal Children's Hospital, Flemington Rd, Parkville, VIC 3052, Australia.

Abstract

Background

There is evolving evidence that vitamin D insufficiency may contribute to food allergy, but findings vary between populations. Lower vitamin D–binding protein (DBP) levels increase the biological availability of serum vitamin D. Genetic polymorphisms explain almost 80% of the variation in binding protein levels.

Objective

We sought to investigate whether polymorphisms that lower the DBP could compensate for adverse effects of low serum vitamin D on food allergy risk.

Methods

From a population-based cohort study (n = 5276) we investigated the association between serum 25-hydroxyvitamin D3 (25[OH]D3) levels and food allergy at age 1 year (338 challenge-proven food-allergic and 269 control participants) and age 2 years (55 participants with persistent and 50 participants with resolved food allergy). 25(OH)D3 levels were measured using liquid chromatography-tandem mass spectrometry and adjusted for season of blood draw. Analyses were stratified by genotype at rs7041 as a proxy marker of DBP levels (low, the GT/TT genotype; high, the GG genotype).

Results

Low serum 25(OH)D3 level (≤50 nM/L) at age 1 years was associated with food allergy, particularly among infants with the GG genotype (odds ratio [OR], 6.0; 95% CI, 0.9-38.9) but not in those with GT/TT genotypes (OR, 0.7; 95% CI, 0.2-2.0; P interaction = .014). Maternal antenatal vitamin D supplementation was associated with less food allergy, particularly in infants with the GT/TT genotype (OR, 0.10; 95% CI, 0.03-0.41). Persistent vitamin D insufficiency increased the likelihood of persistent food allergy (OR, 12.6; 95% CI, 1.5-106.6), particularly in those with the GG genotype.

Conclusions

Polymorphisms associated with lower DBP level attenuated the association between low serum 25(OH)D3 level and food allergy, consistent with greater vitamin D bioavailability in those with a lower DBP level. This increases the biological plausibility of a role for vitamin D in the development of food allergy.

Le texte complet de cet article est disponible en PDF.

Key words : Food hypersensitivity, vitamin D, food allergy, gene, polymorphism, vitamin D binding protein

Abbreviations used : DBP, GC, OR, 25(OH)D3


Plan


 This work was supported by funding from the National Health and Medical Research Council of Australia (grants 491233 and 1006215), Ilhan Food Allergy Foundation, AnaphylaxiStop, Charles and Sylvia Viertel Medical Research Foundation, and the Victorian Government's Operational Infrastructure Support Program. The study sponsors had no involvement in the study design, collection, analysis, and interpretation of data, writing of the report, or decision to submit the paper for publication.
 Disclosure of potential conflict of interest: J. J. Koplin, J. A. Ellis, M. Panjari, A.-L. Ponsonby, M. C. Matheson, A. Lowe, L. C. Gurrin, M. Wake, and S. C. Dharmage are supported by the National Health and Medical Research Council. N. J. Osborne is supported by the European Regional Development Fund and the European Social Fund Convergence Programme, has received grants and travel support from the National Health and Medical Research Council, and has received grants from the Australian Egg Corporation. M. L. K. Tang is on the Medical Advisory Board – Oceania for the Nestlè Nutrition Institute, on the Medical Advisory Board – Australasia, and on the Global Scientific Advisory Board for Danone Nutricia; has consultant arrangements with Deerfield Institute and Gerson Lehrman Group; has received payment for lectures from Danone Nutricia; has a patent on a method for inducing tolerance; has received author royalties from Wiley; has received speakers fees from Nutricia, Nestlè Nutrition Institute, and Wyeth; and has received payment for the development of educational presentations from MD Linx. M. Wake has received research support from the National Health and Medical Research Council. K. J. Allen is supported by the National Health and Medical Research Council; is a Viertel Senior Medical Research Fellow; and has received payment for lectures from Danone, Nestlè, Alphapharm, Abbott, Wyeth, and Nutricia. The rest of the authors declare that they have no relevant conflicts of interest.


© 2015  American Academy of Allergy, Asthma & Immunology. Publié par Elsevier Masson SAS. Tous droits réservés.
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