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Notes: Background Seasonal allergic rhinitis (SAR) is a risk factor for asthma in affected individuals. Nasal allergic inflammation enhances bone-marrow eosinophil production, mainly via IL-5, and rhinitis patients have increased airway inflammation during the pollen season.Objective To assess the impact of nasal allergy on sputum inflammatory markers.Methods In an open-labelled, randomized, placebo-controlled cross-over study with 16 non-asthmatic SAR patients (median age 25 years, 56% males), the effect of a single nasal allergen challenge performed out of season on induced sputum inflammatory parameters was evaluated. SAR patients were identified by history, skin-prick test and specific IgE. All patients had normal lung function/bronchial hyper-responsiveness out of season and a negative asthma/wheezing history. Sputum cells and supernatant levels of ECP, sICAM, IL-5 and IL-10, and plasma levels of IL-5 and ECP, were measured before and 24 h after nasal allergen challenge. After a washout period of at least 4 weeks, the procedure was repeated with placebo challenge (diluent).Results Nasal allergen challenge led to an increase in sputum ECP (pre = 60 ± 12, post = 212 ± 63 µg/L, P = 0.02 vs. placebo), and sICAM (4.8 ± 2.7 to 6.5 ± 2.9 ng/mL, P = 0.02 vs. placebo), whereas IL-10 decreased after provocation (44 ± 11 to 29 ± 6 pg/mL, P = 0.06 vs. placebo). Sputum IL-5 was undetectable in all patients. The absolute number of blood and sputum eosinophils did not change significantly after allergen or placebo challenge (P 〉 0.07, both comparisons). Plasma levels of IL-5 increased after allergen challenge (8.7 ± 2.9 to 14.5 ± 3.9 pg/mL, P = 0.001), and the increase in plasma IL-5 was positively correlated with the rise in sputum ECP in a subgroup of ‘responders’ (n = 12, r = 0.71, P = 0.01).Conclusions A single nasal allergen challenge in SAR patients increased markers of allergic inflammation in the lower respiratory tract, possibly via pronounced activation of inflammatory cells through circulating immediate-type reaction cytokines like IL-5. These findings may provide additional explanatory data for the high susceptibility of SAR patients to incident asthma.