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Journal of clinical medicine · 2026

Circulating Interleukin-17 Across Airway Disease Phenotypes: A Single-Center Observational Study.

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Porr Corina, Iovin Valentin-Cristian, Vidrighin Anca, Preda Emi M, Iancu Gabriela Mariana, Harris Dana M, Diaconu Cosmina

Аннотация

Background: Interleukin-17 (IL-17) contributes to persistent airway inflammation, neutrophil recruitment, and inflammatory pathways extending beyond classical type 2 immunity. However, the distribution of circulating IL-17 across clinically distinct upper- and lower-airway disease phenotypes remains incompletely characterized. This study compared serum IL-17 concentrations in allergic rhinitis, non-allergic asthma, allergic asthma associated with allergic rhinitis, and healthy controls. Methods: This retrospective single-center observational study included 88 adults: allergic rhinitis (n = 31), non-allergic asthma (n = 15), allergic asthma associated with allergic rhinitis (n = 22), and healthy controls (n = 20). Serum IL-17 concentrations were measured using a quantitative sandwich enzyme-linked immunosorbent assay. Overall group differences were assessed using the Kruskal-Wallis test, followed by Holm-adjusted pairwise Mann-Whitney U tests. Results: Serum IL-17 concentrations differed significantly across the four groups (Kruskal-Wallis H = 12.981, p = 0.0047). Median IL-17 concentrations were 126.21 pg/mL in non-allergic asthma, 50.97 pg/mL in allergic rhinitis, 54.72 pg/mL in allergic asthma associated with allergic rhinitis, and 0.00 pg/mL in healthy controls. Each disease group had significantly higher IL-17 than controls after Holm correction (adjusted p = 0.0103, 0.0172, and 0.0196, respectively), whereas the three disease phenotypes did not differ significantly from one another. Conclusions: Circulating IL-17 concentrations were higher in allergic rhinitis, non-allergic asthma, and allergic asthma associated with allergic rhinitis than in healthy controls. However, the substantial overlap among disease phenotypes and the absence of statistically significant between-phenotype differences should not be interpreted as evidence of equivalence or a shared biological mechanism. These findings should be considered exploratory and require confirmation in larger, prospectively characterized cohorts.