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Atopic sensitization in the first year of life - 27/02/13

Doi : 10.1016/j.jaci.2012.11.048 
Martin Depner, PhD a, , Markus J. Ege, MD a, , Jon Genuneit, MD b, Juha Pekkanen, MD, PhD c, d, Marjut Roponen, PhD e, Maija-Riitta Hirvonen, PhD c, e, Jean-Charles Dalphin, MD, PhD f, Vincent Kaulek, PhD f, Susanne Krauss-Etschmann, MD a, g, Josef Riedler, MD h, Charlotte Braun-Fahrländer, MD i, j, Caroline Roduit, MD, MPH k, Roger Lauener, MD k, Petra I. Pfefferle, PhD, DPH l, Juliane Weber, MD a, Erika von Mutius, MD a

PASTURE Study Group

  The members of the PASTURE Study Group are listed in the acknowledgments section.

a University Children’s Hospital, Munich, Germany (Member of the German Center for Lung Research) 
b Institute of Epidemiology, University of Ulm, Ulm, Germany 
c Department of Environmental Health, National Institute for Health and Welfare, Kuopio, Finland 
d Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland 
e Department of Environmental Science, University of Eastern Finland, Kuopio, Finland 
f Department of Respiratory Disease, UMR/CNRS 6249 Chrono-environnement, University Hospital of Besançon, Besançon, France 
g Comprehensive Pneumology Center, Helmholtz Center Munich, Munich, Germany 
h Children’s Hospital, Schwarzach, Austria 
i Swiss Tropical and Public Health Institute, Basel, Switzerland 
j University of Basel, Basel, Switzerland 
k University of Zurich, Children’s Hospital, Zurich, Switzerland, and Christine Kühne–Center for Allergy Research and Education, Davos, Switzerland 
l Institute for Laboratory Medicine and Pathobiochemistry, Molecular Diagnostics, Philipps University of Marburg, Marburg, Germany 

Corresponding author: Martin Depner, PhD, Dr. von Haunersche Kinderklinik, Lindwurmstrasse 4, 80337 Munich, Germany.

Abstract

Background

There is conflicting evidence on whether allergen-specific memory is primed prenatally, whether this priming affects persistent immunologic effects, and whether it is modulated by the first environmental exposures in infancy.

Objective

We sought to explore the course of atopic sensitization between birth and 12 months of age.

Methods

Specific IgE levels for 6 food and 13 common inhalant allergens were assessed in cord blood and 1-year blood samples in the Protection against Allergy–Study in Rural Environments (PASTURE) birth cohort including 793 children from rural regions of 5 European countries. Detailed information on children’s health, nutrition, and farm-related exposures was gathered by using a pregnancy questionnaire, 2 questionnaires at 2 and 12 months of age, and a diary covering the time in between.

Results

Sensitization was more common at 12 months of age than at birth for almost all specificities. On an individual level, persistent sensitization to the same allergens was rare (1%), whereas transient (only at birth, 11%) and incident (only at 12 months, 34%) sensitization was seen in substantial proportions of children. Associations of transient sensitization with maternal sensitization differed with the allergen specificities, with the strongest associations for food allergens (odds ratio [OR], 10.6; 95% CI, 6.0-18.6) and the weakest associations for seasonal allergens (OR, 1.64; 95% CI, 0.94-2.86). Associations of maternal sensitization with incident sensitization were also seen. Incident sensitization was related to distinct prenatal and postnatal environmental exposures of mother and child, such as consumption of cereals for incident sensitization to seasonal allergens (OR, 0.66; 95% CI, 0.50-0.88).

Conclusion

IgE sensitization patterns change between birth and 12 months and are related to maternal and environmental influences.

Le texte complet de cet article est disponible en PDF.

Key words : Atopic sensitization, early life, environmental exposures

Abbreviations used : aOR, PARSIFAL, PASTURE, OR


Plan


 Supported by the European Commission (research grants QLK4-CT-2001-00250, FOOD-CT-2006-31708, and KBBE-2007-2-2-06).
 Disclosure of potential conflict of interest: M. Depner has received grants from the European Research Council. M. J. Ege has received grants from the European Commission. M. Roponen and M.-R. Hirvonen have received grants from the European Union. J.-C. Dalphin has received grants and travel support from the French Ministry of Health and the European Community; has received writing assistance, medicine, equipment, or administrative support from the French Society of Respiratory Diseases; is a board member for Novartis; has received grants from GlaxoSmithKline; has received payment for lectures from Novartis, GlaxoSmithKline, AstraZeneca, and Chiesi; has received payment for development of educational presentations from Novartis; and has received travel support from GlaxoSmithKline, Novartis, AstraZeneca, and Chiesi. R. Lauener has received grants, travel support, and fees for participation in review activities from the European Union and the Kühne Foundation and has received payment for lectures from Phadia–Thermo Fisher. J. Weber has received grants from the European Commission. E. von Mutius has received grants from the European Commission, the European Research Council, the German Research Foundation, and the German Federal Ministry of Education and Research. M. Kabesch has received a grant from the European Union and has received payment for lectures from the European Respiratory Society, the European Academy of Allergy and Clinical Immunology, the American Thoracic Society, Novartis, and GlaxoSmithKline. G. Doekes has received grants and travel support from the European Union Commission. B. Schaub has received grants from the German Research Foundation. The rest of the authors declare that they have no relevant conflicts of interest.


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