胸腺基质淋巴细胞生成素
医学
慢性阻塞性肺病
粘液
嗜酸性粒细胞
免疫学
气道
炎症
内科学
外科
生物
生态学
哮喘
作者
Alejandro A. Díaz,Scott Grumley,Andrew Yen,Sushilkumar K. Sonavane,Rim Elalami,M Abdalla,Kangjin Kim,Pietro Nardelli,Sharon S. Brouha,Padma P. Manapragada,Mostafa Abozeed,Muhammad Usman Aziz,M. Zahid,Hrudaya Nath,Wei Wang,James C. Ross,Carrie P. Aaron,Raúl San Jośe Estépar,Michael H. Cho
出处
期刊:The European respiratory journal
[European Respiratory Society]
日期:2024-11-21
卷期号:: 2401005-2401005
标识
DOI:10.1183/13993003.01005-2024
摘要
Extract Type 2 inflammation (Th2i) —indicated by blood eosinophil counts— and airway-occluding mucus plugs (MPs) on computed tomography (CT) are frequent phenotypes in people with COPD. [1–4] Furthermore, the Th2i pathway involves type 2 helper T cells and epithelial-derived cytokines, such as interleukin (IL-) 33 and thymic stromal lymphopoietin (TSLP), that drive a cascade of events, including eosinophils mobilization and activation in the airways. [5] A persistent Th2i milieu leads to airway structural changes, such as mucus gland hypertrophy, ensuing mucus hypersecretion, and plug formation. [5, 6] Therefore, we tested the hypothesis that high blood eosinophils are associated with airway MPs. We also sought to determine the association of those phenotypes with functional and clinical measures of COPD.
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