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气道疾病表型中的循环白细胞介素-17:一项单中心观察性研究

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

临床研究鼻科IF 3.5Q1

文献信息

中文摘要

背景: 白细胞介素-17(IL-17)参与持续性气道炎症、中性粒细胞募集以及超出经典2型免疫的炎症通路。然而,循环IL-17在临床不同的上气道和下气道疾病表型中的分布仍未得到充分表征。本研究比较了过敏性鼻炎、非过敏性哮喘、伴过敏性鼻炎的过敏性哮喘以及健康对照者的血清IL-17浓度。
方法: 这项回顾性单中心观察性研究纳入88名成人:过敏性鼻炎(n = 31)、非过敏性哮喘(n = 15)、伴过敏性鼻炎的过敏性哮喘(n = 22)以及健康对照者(n = 20)。使用定量夹心酶联免疫吸附测定法测量血清IL-17浓度。总体组间差异采用Kruskal-Wallis检验评估,随后进行Holm校正的成对Mann-Whitney U检验。
结果: 四组间血清IL-17浓度存在显著差异(Kruskal-Wallis H = 12.981,p = 0.0047)。IL-17浓度中位数在非过敏性哮喘中为126.21 pg/mL,在过敏性鼻炎中为50.97 pg/mL,在伴过敏性鼻炎的过敏性哮喘中为54.72 pg/mL,在健康对照者中为0.00 pg/mL。经Holm校正后,每个疾病组的IL-17均显著高于对照者(校正后p = 0.0103、0.0172和0.0196),而三种疾病表型之间无显著差异。
结论: 过敏性鼻炎、非过敏性哮喘以及伴过敏性鼻炎的过敏性哮喘患者的循环IL-17浓度高于健康对照者。然而,疾病表型之间的显著重叠以及表型间无统计学显著差异不应被解释为等效性或共享生物学机制的证据。这些发现应被视为探索性结果,并需要在更大规模、前瞻性表征的队列中加以确认。

英文摘要

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.