BACKGROUND: IgE sensitization against grass pollen is a cause of seasonal allergic rhinitis. OBJECTIVE: We sought to investigate the evolution at the molecular level and the preclinical predictive value of IgE responses against grass pollen. METHODS: The German Multicentre Allergy Study examined a birth cohort born in 1990. A questionnaire was administered yearly, and blood samples were collected at 1, 2, 3, 5, 6, 7, 10, and 13 years of age. Grass pollen-related seasonal allergic rhinitis (SARg) was diagnosed according to nasal symptoms in June/July. Serum IgE antibodies to Phleum pratense extract and 8 P pratense molecules were tested with immune-enzymatic singleplex and multiplex assays, respectively. RESULTS: One hundred seventy-seven of the 820 examined children had SARg. A weak monomolecular/oligomolecular IgE response to P pratense was observed very frequently before SARg onset. These initial IgE responses increased in concentration and molecular complexity during the preclinical and clinical process. A typical progression of IgE sensitization was observed: Phl p 1 (initiator in >75% of cases); then Phl p 4 and Phl p 5; then Phl p 2, Phl p 6, and Phl p 11; and then Phl p 12 and Phl p 7. At age 3 years, IgE sensitization predicted SARg by age 12 years (positive predictive value, 68% [95% CI, 50% to 82%]; negative predictive value, 84% [95% CI, 80% to 87%]). At this preclinical prediction time, the number of recognized molecules and the serum levels of IgE to P pratense were significantly lower than at 3 or more years after SARg onset. CONCLUSIONS: The IgE response against grass pollen molecules can start years before disease onset as a weak monosensitization or oligosensitization phenomenon. It can increase in serum concentration and complexity through a "molecular spreading" process during preclinical and early clinical disease stages. Testing IgE sensitization at a preclinical stage facilitates prediction of seasonal allergic rhinitis at its molecular monosensitization or oligosensitization stage.
BACKGROUND: IgE sensitization against grass pollen is a cause of seasonal allergic rhinitis. OBJECTIVE: We sought to investigate the evolution at the molecular level and the preclinical predictive value of IgE responses against grass pollen. METHODS: The German Multicentre Allergy Study examined a birth cohort born in 1990. A questionnaire was administered yearly, and blood samples were collected at 1, 2, 3, 5, 6, 7, 10, and 13 years of age. Grass pollen-related seasonal allergic rhinitis (SARg) was diagnosed according to nasal symptoms in June/July. Serum IgE antibodies to Phleum pratense extract and 8 P pratense molecules were tested with immune-enzymatic singleplex and multiplex assays, respectively. RESULTS: One hundred seventy-seven of the 820 examined children had SARg. A weak monomolecular/oligomolecular IgE response to P pratense was observed very frequently before SARg onset. These initial IgE responses increased in concentration and molecular complexity during the preclinical and clinical process. A typical progression of IgE sensitization was observed: Phl p 1 (initiator in >75% of cases); then Phl p 4 and Phl p 5; then Phl p 2, Phl p 6, and Phl p 11; and then Phl p 12 and Phl p 7. At age 3 years, IgE sensitization predicted SARg by age 12 years (positive predictive value, 68% [95% CI, 50% to 82%]; negative predictive value, 84% [95% CI, 80% to 87%]). At this preclinical prediction time, the number of recognized molecules and the serum levels of IgE to P pratense were significantly lower than at 3 or more years after SARg onset. CONCLUSIONS: The IgE response against grass pollen molecules can start years before disease onset as a weak monosensitization or oligosensitization phenomenon. It can increase in serum concentration and complexity through a "molecular spreading" process during preclinical and early clinical disease stages. Testing IgE sensitization at a preclinical stage facilitates prediction of seasonal allergic rhinitis at its molecular monosensitization or oligosensitization stage.
Authors: Wendy F Davidson; Donald Y M Leung; Lisa A Beck; Cecilia M Berin; Mark Boguniewicz; William W Busse; Talal A Chatila; Raif S Geha; James E Gern; Emma Guttman-Yassky; Alan D Irvine; Brian S Kim; Heidi H Kong; Gideon Lack; Kari C Nadeau; Julie Schwaninger; Angela Simpson; Eric L Simpson; Jonathan M Spergel; Alkis Togias; Ulrich Wahn; Robert A Wood; Judith A Woodfolk; Steven F Ziegler; Marshall Plaut Journal: J Allergy Clin Immunol Date: 2019-01-09 Impact factor: 10.793
Authors: Miguel Tortajada-Girbés; María Mesa Del Castillo; Helena Larramona; José Manuel Lucas; Montserrat Álvaro Lozano; Ana Isabel Tabar; Begoña Soler López; Ana Martínez-Cañavate Journal: Eur J Pediatr Date: 2019-08-14 Impact factor: 3.183
Authors: Christoph Madritsch; Elisabeth Gadermaier; Uwe W Roder; Christian Lupinek; Rudolf Valenta; Sabine Flicker Journal: J Immunol Date: 2015-01-30 Impact factor: 5.422
Authors: Marit Westman; Christian Lupinek; Jean Bousquet; Niklas Andersson; Sandra Pahr; Alexandra Baar; Anna Bergström; Mats Holmström; Pär Stjärne; Karin C Lødrup Carlsen; Kaj-Håkon Carlsen; Josep M Antó; Rudolf Valenta; Marianne van Hage; Magnus Wickman Journal: J Allergy Clin Immunol Date: 2014-12-18 Impact factor: 10.793