A single nasal allergen challenge increases induced sputum inflammatory markers in non-asthmatic subjects with seasonal allergic rhinitis: correlation with plasma interleukin-5

Summary 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.