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Fixed airflow obstruction relates to eosinophil activation in asthmatics

机译：固定气流阻塞涉及哮喘症的嗜酸性粒细胞激活

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Background Some asthmatics develop irreversible chronic airflow obstruction, for example, fixed airflow obstruction (fixed-AO). This is probably a consequence of airway remodelling, but neither its relation to inflammation nor which asthma biomarkers can be clinically useful are elucidated. We hypothesized that the presence of type 2 inflammation relates to fixed-AO. Objectives To evaluate the presence of four markers for type 2 inflammation in fixed airflow obstruction among asthmatics. Methods This was a cross-sectional study of 403 participants with asthma, aged 17-75 years, from three Swedish centres. Fixed airflow obstruction was defined as forced expiratory volume during the first second (FEV1) over forced vital capacity (FVC) being below the lower limit of normal (LLN). The following type 2 inflammation markers were assessed: exhaled nitric oxide (FeNO), serum periostin, serum eosinophil cationic protein (S-ECP), and urinary eosinophil-derived neurotoxin (U-EDN). Results Elevated U-EDN (values in the highest tertile, = 65.95 mg/mol creatinine) was more common in subjects with fixed-AO vs. subjects without fixed-AO: 55% vs. 29%, P EDN related to increased likelihood of having fixed-AO in both all subjects and never-smoking subjects, with adjusted (adjusted for sex, age group, use of inhaled corticosteroids last week, atopy, early-onset asthma, smoking history, and packyears) odds ratios (aOR) of 2.38 (1.28-4.41) and 2.51 (1.04-6.07), respectively. In a separate analysis, having both elevated S-ECP (20 mu g/L) and U-EDN was related to having the highest likelihood of fixed-AO (aOR (95% CI) 6.06 (2.32-15.75)). Elevated serum periostin or FeNO did not relate to fixed-AO. Conclusions and clinical relevance These findings support that type 2 inflammation, and in particular eosinophil inflammation, is found in asthma with fixed-AO. This could indicate a benefit from eosinophil-directed therapies. Further longitudinal studies are warranted to investigate causality and relation to lung function decline.
机译：背景技术一些哮喘产生不可逆的慢性气流阻塞，例如固定气流阻塞（固定AO）。这可能是气道重塑的结果，但既不是炎症的关系也不是临床上有用的。我们假设2型炎症的存在涉及固定AO。目的是评估哮喘中固定气流阻塞中2型炎症的四个标记的存在。方法这是来自三名瑞典中心的403名哮喘的参与者的横截面研究。固定气流梗阻被定义为在第一秒（FEV1）期间强制急性容量（FVC）的强制呼气量低于正常（LLN）的下限。评估以下2型炎症标志物：呼出的一氧化氮（FENO），血清肝蛋蛋白，血清嗜酸性粒细胞阳离子蛋白（S-ECP）和泌尿嗜酸性粒细胞衍生的神经毒素（U-EDN）。结果升高的U-EDN（最高触角的值，＆ = 65.95 mg / mol肌酐）在没有固定AO的固定AO与受试者的受试者中更常见：55％与29％，P EDN与增加相关在所有受试者和从不吸烟的受试者中具有固定AO的可能性，调整（对性别，年龄组调整，上周使用吸入的皮质类固醇，Atopt，早期哮喘，吸烟历史和包装阶段）的差异比例（AOR ）分别为2.38（1.28-4.41）和2.51（1.04-6.07）。在单独的分析中，具有升高的S-ECP（＆20μg/ L）和U-EDN与固定AO（AOR（95％CI）6.06（2.32-15.75）的可能性有关。升高的血清骨膜或FENO与固定AO无关。结论和临床关联这些发现支持2型炎症，特别是嗜酸性粒细胞炎症，在哮喘中发现了固定AO。这可能表明来自嗜酸性粒细胞导向的疗法的益处。需要进一步纵向研究来调查因果关系和与肺功能下降的关系。

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