Stephanie Hofmaier1, Laura Hatzler1, Alexander Rohrbach1, Valentina Panetta2, Dani Hakimeh1, Carl Peter Bauer3, Ute Hoffman3, Johannes Forster4, Fred Zepp5, Antje Schuster6, Philippe Stock1, Ulrich Wahn1, Thomas Keil7, Susanne Lau1, Paolo Maria Matricardi8. 1. Department of Paediatric Pneumology & Immunology, Charité-Universitätsmedizin Berlin, Berlin, Germany. 2. L'altrastatistica srl, Consultancy & Training, Biostatistics Office, Rome, Italy. 3. Department of Pediatrics, Technical University of Munich, Munich, Germany. 4. Department of Pediatrics St Hedwig, St Josefs Hospital, Freiburg, Germany. 5. Department of Pediatrics and Adolescent Medicine, Johannes Gutenberg University Medical Centre, Mainz, Germany. 6. Department of Pediatric Cardiology and Pneumology, Heinrich-Heine-University, Düsseldorf, Germany. 7. Institute of Social Medicine, Epidemiology and Health Economics, Charité-Universitätsmedizin Berlin, Berlin, Germany; Institute of Clinical Epidemiology and Biometry, University of Würzburg, Würzburg, Germany. 8. Department of Paediatric Pneumology & Immunology, Charité-Universitätsmedizin Berlin, Berlin, Germany. Electronic address: paolo.matricardi@charite.de.
Abstract
BACKGROUND: The route and dose of exposure are believed to be relevant factors in the sensitization process. Pathogenesis-related group 10 protein (PR-10) molecules are a family of allergenic proteins shared by many pollens (eg, birch and alder) and foods (eg, apple, peach, and soy). Children are exposed to both pollen-derived (inhaled) and food-derived (ingested) PR-10 molecules. OBJECTIVE: We sought to investigate the role of route and dose of exposure in the evolution of IgG and IgE responses to recombinant PR-10 molecules. METHODS: The German Multicentre Allergy Study examined a birth cohort born in 1990. Blood samples were collected at the ages of 1, 2, 3, 5, 6, 7, 10, and 13 years. Participants were included in the present analysis if they had (1) at least 1 serum sample at each of the 4 age periods or time points (1-3 years, 5-7 years, 10 years, and 13 years) and (2) IgE responses to birch (children with birch atopy) or no IgE response at all to 9 common aeroallergens and food allergens (nonatopic children). Therefore serum IgE antibodies to a panel of 4 airborne and 5 foodborne extracts, as well as to Bet v 1, were measured in singleplex assays, whereas IgG and IgE antibodies to a panel of 3 airborne PR-10 molecules (rBet v 1, rAln g 1, and rCor a 1.0101) and 7 foodborne PR-10 molecules (rCor a 1.0401, rMal d 1, rPru p 1, rGly m 4, rAra h 8, rApi g 1, and rDau c 1) were tested by using a multiplex microarray. RESULTS: In the present analyses we included 28 children with birch atopy and randomly selected 28 nonatopic children from the 190 children fulfilling the inclusion criteria. Two different patterns of IgG responses to PR-10 molecules were identified. Among nonatopic subjects, a "default" IgG response was directed mostly against foodborne PR-10, started often before age 2 years, stayed weak, and was mostly transient. Among all atopic subjects, the default IgG response at age 1 year was overwhelmed after age 2 years by an "pre-atopic" IgG response, which started with or shortly before the IgE response and was intense and persistent. This atopic IgG response, as well as the IgE response, involved progressively more foodborne PR-10 proteins with frequencies and levels related to their homology with Bet v 1. CONCLUSIONS: The results suggest that children have a default antibody response to PR-10 molecules, which is early, weak, and transient; does not involve IgE; and is initiated by foodborne PR-10. By contrast, an atopic antibody response to PR-10 molecules is delayed, strong, and persistent; involves both IgG and IgE; and is initiated by airborne PR-10.
BACKGROUND: The route and dose of exposure are believed to be relevant factors in the sensitization process. Pathogenesis-related group 10 protein (PR-10) molecules are a family of allergenic proteins shared by many pollens (eg, birch and alder) and foods (eg, apple, peach, and soy). Children are exposed to both pollen-derived (inhaled) and food-derived (ingested) PR-10 molecules. OBJECTIVE: We sought to investigate the role of route and dose of exposure in the evolution of IgG and IgE responses to recombinant PR-10 molecules. METHODS: The German Multicentre Allergy Study examined a birth cohort born in 1990. Blood samples were collected at the ages of 1, 2, 3, 5, 6, 7, 10, and 13 years. Participants were included in the present analysis if they had (1) at least 1 serum sample at each of the 4 age periods or time points (1-3 years, 5-7 years, 10 years, and 13 years) and (2) IgE responses to birch (children with birch atopy) or no IgE response at all to 9 common aeroallergens and food allergens (nonatopic children). Therefore serum IgE antibodies to a panel of 4 airborne and 5 foodborne extracts, as well as to Bet v 1, were measured in singleplex assays, whereas IgG and IgE antibodies to a panel of 3 airborne PR-10 molecules (rBet v 1, rAln g 1, and rCor a 1.0101) and 7 foodborne PR-10 molecules (rCor a 1.0401, rMal d 1, rPru p 1, rGly m 4, rAra h 8, rApi g 1, and rDau c 1) were tested by using a multiplex microarray. RESULTS: In the present analyses we included 28 children with birch atopy and randomly selected 28 nonatopic children from the 190 children fulfilling the inclusion criteria. Two different patterns of IgG responses to PR-10 molecules were identified. Among nonatopic subjects, a "default" IgG response was directed mostly against foodborne PR-10, started often before age 2 years, stayed weak, and was mostly transient. Among all atopic subjects, the default IgG response at age 1 year was overwhelmed after age 2 years by an "pre-atopic" IgG response, which started with or shortly before the IgE response and was intense and persistent. This atopic IgG response, as well as the IgE response, involved progressively more foodborne PR-10 proteins with frequencies and levels related to their homology with Bet v 1. CONCLUSIONS: The results suggest that children have a default antibody response to PR-10 molecules, which is early, weak, and transient; does not involve IgE; and is initiated by foodborne PR-10. By contrast, an atopic antibody response to PR-10 molecules is delayed, strong, and persistent; involves both IgG and IgE; and is initiated by airborne PR-10.
Authors: Luis Caraballo; Josefina Zakzuk; Bee Wah Lee; Nathalie Acevedo; Jian Yi Soh; Mario Sánchez-Borges; Elham Hossny; Elizabeth García; Nelson Rosario; Ignacio Ansotegui; Leonardo Puerta; Jorge Sánchez; Victoria Cardona Journal: World Allergy Organ J Date: 2016-06-27 Impact factor: 4.084
Authors: Huey-Jy Huang; Raffaela Campana; Oluwatoyin Akinfenwa; Mirela Curin; Eszter Sarzsinszky; Antonina Karsonova; Ksenja Riabova; Alexander Karaulov; Katarzyna Niespodziana; Olga Elisyutina; Elena Fedenko; Alla Litovkina; Evgenii Smolnikov; Musa Khaitov; Susanne Vrtala; Thomas Schlederer; Rudolf Valenta Journal: Front Immunol Date: 2021-02-12 Impact factor: 7.561
Authors: Inna Tulaeva; Bernhard Kratzer; Raffaela Campana; Mirela Curin; Marianne van Hage; Antonina Karsonova; Ksenja Riabova; Alexander Karaulov; Musa Khaitov; Winfried F Pickl; Rudolf Valenta Journal: Front Immunol Date: 2020-07-07 Impact factor: 7.561