Marit Westman1, Christian Lupinek2, Jean Bousquet3, Niklas Andersson4, Sandra Pahr2, Alexandra Baar2, Anna Bergström4, Mats Holmström5, Pär Stjärne5, Karin C Lødrup Carlsen6, Kaj-Håkon Carlsen6, Josep M Antó7, Rudolf Valenta2, Marianne van Hage8, Magnus Wickman9. 1. Department of Clinical Science, Intervention and Technology, Division of Ear, Nose and Throat Diseases, Karolinska Institutet, Stockholm, Sweden; Department of Ear, Nose and Throat Diseases, Karolinska University Hospital, Stockholm, Sweden. Electronic address: marit.westman@ki.se. 2. Division of Immunopathology, Department of Pathophysiology and Allergy Research, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria. 3. University Hospital of Montpellier, Hôpital Arnaud de Villeneuve, Montpellier, INSERM 1018, Villejuif, France. 4. Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. 5. Department of Clinical Science, Intervention and Technology, Division of Ear, Nose and Throat Diseases, Karolinska Institutet, Stockholm, Sweden; Department of Ear, Nose and Throat Diseases, Karolinska University Hospital, Stockholm, Sweden. 6. Department of Pediatrics, University of Oslo, Oslo University Hospital, Oslo, Norway. 7. Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain; IMIM (Hospital del Mar Research Institute), Barcelona, Spain; Universitat Pompeu Fabra (UPF), Barcelona, Spain; CIBER Epidemiología y Salud Pública (CIBERESP), Barcelona, Spain. 8. Clinical Immunology and Allergy Unit, Department of Medicine Solna, Karolinska Institutet and University Hospital, Stockholm, Sweden. 9. Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden; Sachs' Children's Hospital, Södersjukhuset, Stockholm, Sweden.
Abstract
BACKGROUND: Component-resolved diagnosis might improve the prediction of future allergy in young children. OBJECTIVE: We sought to investigate the association between IgE reactivity to the pathogenesis-related class 10 (PR-10) protein family and allergic rhinitis to birch pollen (ARbp) from early childhood up to age 16 years. METHOD: Questionnaire data and sera obtained at 4, 8, and 16 years of age from the Barn/Children Allergi/Allergy Milieu Stockholm Epidemiologic (BAMSE) study birth cohort were used. Sera from 764 children were analyzed for IgE reactivity to 9 PR-10 allergen proteins at the 3 time points by using an allergen chip based on ISAC technology. ARbp was defined as upper airway symptoms during birch pollen exposure. RESULTS: IgE reactivity to Bet v 1 was found in 12%, 17%, and 25% of children at 4, 8, and 16 years of age. IgE reactivity of PR-10 proteins showed a hierarchic intrarelationship: Bet v 1 > Mal d 1 > Cor a 1.04 > Ara h 8 > Pru p 1 > Aln g 1 > Api g 1 > Act d 8 > Gly m 4. There was an increased risk of incidence and persistence of ARbp up to age 16 years with increasing levels of Bet v 1-specific IgE or increasing numbers of IgE-reactive PR-10 proteins at 4 years. Children with severe ARbp at age 16 years had higher levels of Bet v 1-specific IgE at age 4 years compared with children with mild symptoms. CONCLUSION: ARbp at age 16 years can be predicted by analysis of IgE reactivity to PR-10 proteins in early childhood.
BACKGROUND: Component-resolved diagnosis might improve the prediction of future allergy in young children. OBJECTIVE: We sought to investigate the association between IgE reactivity to the pathogenesis-related class 10 (PR-10) protein family and allergic rhinitis to birch pollen (ARbp) from early childhood up to age 16 years. METHOD: Questionnaire data and sera obtained at 4, 8, and 16 years of age from the Barn/Children Allergi/Allergy Milieu Stockholm Epidemiologic (BAMSE) study birth cohort were used. Sera from 764 children were analyzed for IgE reactivity to 9 PR-10 allergen proteins at the 3 time points by using an allergen chip based on ISAC technology. ARbp was defined as upper airway symptoms during birch pollen exposure. RESULTS: IgE reactivity to Bet v 1 was found in 12%, 17%, and 25% of children at 4, 8, and 16 years of age. IgE reactivity of PR-10 proteins showed a hierarchic intrarelationship: Bet v 1 > Mal d 1 > Cor a 1.04 > Ara h 8 > Pru p 1 > Aln g 1 > Api g 1 > Act d 8 > Gly m 4. There was an increased risk of incidence and persistence of ARbp up to age 16 years with increasing levels of Bet v 1-specific IgE or increasing numbers of IgE-reactive PR-10 proteins at 4 years. Children with severe ARbp at age 16 years had higher levels of Bet v 1-specific IgE at age 4 years compared with children with mild symptoms. CONCLUSION: ARbp at age 16 years can be predicted by analysis of IgE reactivity to PR-10 proteins in early childhood.
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