Mareen R Datema1, Laurian Zuidmeer-Jongejan1, Riccardo Asero2, Laura Barreales3, Simona Belohlavkova4, Frédéric de Blay5, Peter Bures6, Michael Clausen7, Ruta Dubakiene8, David Gislason7, Monika Jedrzejczak-Czechowicz9, Marek L Kowalski9, André C Knulst10, Tanya Kralimarkova11, Thuy-My Le10, Alison Lovegrove12, Justin Marsh13, Nikolaos G Papadopoulos14, Todor Popov15, Náyade Del Prado3, Ashok Purohit5, Gerald Reese15, Isabel Reig16, Suranjith L Seneviratne17, Athanasios Sinaniotis18, Serge A Versteeg1, Stefan Vieths15, Aeilko H Zwinderman19, Clare Mills13, Jonas Lidholm20, Karin Hoffmann-Sommergruber21, Montserrat Fernández-Rivas16, Barbara Ballmer-Weber6, Ronald van Ree22. 1. Department of Experimental Immunology, Academic Medical Center, Amsterdam, The Netherlands. 2. Ambulatorio di Allergologia, Clinica San Carlo, Paderno Dugnano, Italy. 3. Clinical Epidemiology Unit, Preventive Medicine Department, Hospital Clinico San Carlos, IdISSC, Madrid, Spain. 4. Pediatric Department, Faculty Hospital Bulovka, Prague, Czech Republic. 5. Allergy Division, Chest Disease Department, University Hospital of Strasbourg, Strasbourg, France. 6. Allergy Unit, Department of Dermatology, University Hospital Zürich, Zürich, Switzerland. 7. Faculty of Medicine, University of Iceland, Landspitali University Hospital, Reykjavik, Iceland. 8. Medical Faculty, Vilnius University, Vilnius, Lithuania. 9. Department of Immunology, Rheumatology and Allergy, Faculty of Medicine, Medical University of Lodz, Lodz, Poland. 10. Department of Dermatology and Allergology, University Medical Center Utrecht, Utrecht, The Netherlands. 11. Clinic of Allergy and Asthma, Medical University of Sofia, Sofia, Bulgaria. 12. Department of Plant Biology and Crop Science, Rothamsted Research, Harpenden, United Kingdom. 13. Institute of Inflammation and Repair, Manchester Institute of Biotechnology, University of Manchester, Manchester, United Kingdom. 14. Allergy Department, 2nd Pediatric Clinic, University of Athens, Athens, Greece; Centre for Paediatrics and Child Health, Institute of Human Development, University of Manchester, Manchester, United Kingdom. 15. Division of Allergology, Paul-Ehrlich-Insitut, Federal Institute for Vaccines and Biomedicines, Langen, Germany. 16. Allergy Department, Hospital Clinico San Carlos, IdISSC, Madrid, Spain. 17. Department of Clinical Immunology, St Mary's Hospital, and Imperial College London, London, United Kingdom. 18. Allergy Department, 2nd Pediatric Clinic, University of Athens, Athens, Greece. 19. Department of Clinical Epidemiology, Biostatistics and Bioinformatics, Academic Medical Centre, Amsterdam, The Netherlands. 20. Phadia AB, Uppsala, Sweden. 21. Department of Pathophysiology and Allergy Research, Medical University of Vienna, Vienna, Austria. 22. Department of Experimental Immunology, Academic Medical Center, Amsterdam, The Netherlands; Department of Otorhinolaryngology, Academic Medical Center, Amsterdam, The Netherlands. Electronic address: r.vanree@amc.uva.nl.
Abstract
BACKGROUND: Hazelnut allergy is birch pollen-driven in Northern/Western Europe and lipid transfer protein-driven in Spain and Italy. Little is known about other regions and other allergens. OBJECTIVE: Establishing a molecular map of hazelnut allergy across Europe. METHODS: In 12 European cities, subjects reporting reactions to hazelnut (n = 731) were evaluated and sensitization to 24 foods, 12 respiratory allergen sources, and latex was tested by using skin prick test and ImmunoCAP. A subset (124 of 731) underwent a double-blind placebo-controlled food challenge to hazelnut. Sera of 423 of 731 subjects were analyzed for IgE against 7 hazelnut allergens and cross-reactive carbohydrate determinants by ImmunoCAP. RESULTS: Hazelnut allergy was confirmed in 70% of those undergoing double-blind placebo-controlled food challenges. Birch pollen-driven hazelnut sensitization (Cor a 1) dominated in most cities, except in Reykjavik, Sofia, Athens, and Madrid, where reporting of hazelnut allergy was less frequent anyhow. In Athens, IgE against Cor a 8 dominated and strongly correlated with IgE against walnut, peach, and apple and against Chenopodium, plane tree, and mugwort pollen. Sensitization to seed storage proteins was observed in less than 10%, mainly in children, and correlated with IgE to nuts, seeds, and legumes. IgE to Cor a 12, observed in all cities (10% to 25%), correlated with IgE to nuts, seeds, and pollen. CONCLUSIONS: In adulthood, the importance of hazelnut sensitization to storage proteins, oleosin (Cor a 12), and Cor a 8 is diluted by the increased role of birch pollen cross-reactivity with Cor a 1. Cor a 8 sensitization in the Mediterranean is probably driven by diet in combination with pollen exposure. Hazelnut oleosin sensitization is prevalent across Europe; however, the clinical relevance remains to be established.
BACKGROUND: Hazelnut allergy is birch pollen-driven in Northern/Western Europe and lipid transfer protein-driven in Spain and Italy. Little is known about other regions and other allergens. OBJECTIVE: Establishing a molecular map of hazelnut allergy across Europe. METHODS: In 12 European cities, subjects reporting reactions to hazelnut (n = 731) were evaluated and sensitization to 24 foods, 12 respiratory allergen sources, and latex was tested by using skin prick test and ImmunoCAP. A subset (124 of 731) underwent a double-blind placebo-controlled food challenge to hazelnut. Sera of 423 of 731 subjects were analyzed for IgE against 7 hazelnut allergens and cross-reactive carbohydrate determinants by ImmunoCAP. RESULTS: Hazelnut allergy was confirmed in 70% of those undergoing double-blind placebo-controlled food challenges. Birch pollen-driven hazelnut sensitization (Cor a 1) dominated in most cities, except in Reykjavik, Sofia, Athens, and Madrid, where reporting of hazelnut allergy was less frequent anyhow. In Athens, IgE against Cor a 8 dominated and strongly correlated with IgE against walnut, peach, and apple and against Chenopodium, plane tree, and mugwort pollen. Sensitization to seed storage proteins was observed in less than 10%, mainly in children, and correlated with IgE to nuts, seeds, and legumes. IgE to Cor a 12, observed in all cities (10% to 25%), correlated with IgE to nuts, seeds, and pollen. CONCLUSIONS: In adulthood, the importance of hazelnut sensitization to storage proteins, oleosin (Cor a 12), and Cor a 8 is diluted by the increased role of birch pollen cross-reactivity with Cor a 1. Cor a 8 sensitization in the Mediterranean is probably driven by diet in combination with pollen exposure. Hazelnut oleosin sensitization is prevalent across Europe; however, the clinical relevance remains to be established.
Authors: Sarah A Lyons; Paco M J Welsing; Mariam Hakobyan; Hannah M Kansen; Edward F Knol; Henny G Otten; Ronald van Ree; André C Knulst; Thuy-My Le Journal: Allergy Date: 2021-11-16 Impact factor: 14.710
Authors: F Blanc; H Bernard; S Ah-Leung; L Przybylski-Nicaise; P Stahl Skov; A Purohit; F de Blay; B Ballmer-Weber; P Fritsche; M Fernandez Rivas; I Reig; A Sinaniotis; E Vassilopoulou; K Hoffmann-Sommergruber; S Vieths; N Rigby; C Mills; K Adel-Patient Journal: Clin Transl Allergy Date: 2015-07-17 Impact factor: 5.871
Authors: Diana Margarida Gonçalves Solha Pereira da Silva; Teresa Maria Silva Vieira; Ana Maria Alves Pereira; André Miguel Afonso de Sousa Moreira; José Luís Dias Delgado Journal: Clin Transl Allergy Date: 2016-12-22 Impact factor: 5.871
Authors: Mark A Blankestijn; André C Knulst; Edward F Knol; Thuy-My Le; Heike Rockmann; Henny G Otten; Rob J B Klemans Journal: Clin Transl Allergy Date: 2017-11-23 Impact factor: 5.871