Katalog Plus
Bibliothek der Frankfurt UAS
Bald neuer Katalog: sichern Sie sich schon vorab Ihre persönlichen Merklisten im Nutzerkonto: Anleitung.
Dieses Ergebnis aus BASE kann Gästen nicht angezeigt werden.  Login für vollen Zugriff.

C-BIOPRED severe asthma clinical phenotypes: link to complement and coagulation pathways and galectin 10

Title: C-BIOPRED severe asthma clinical phenotypes: link to complement and coagulation pathways and galectin 10
Authors: Changxing Ou; Zhenan Deng; Yongkang Liao; Xiaomin Cen; Penghui Wu; Chenyang Lu; Xiuhua Fu; Changzheng Wang; Meilin Jin; Guochao Shi; Zhongmin Qiu; Xiaoyang Wei; Wei Gu; Jian Kang; Yunhui Zhang; Mao Huang; Jinfu Xu; Kewu Huang; Qiang Li; Xiangyan Zhang; Chunhua Wei; Guangfa Wang; Kian Fan Chung; Nanshan Zhong; Qingling Zhang; Jiaxing Xie
Source: ERJ Open Research, Vol 11, Iss 4 (2025)
Publisher Information: European Respiratory Society
Publication Year: 2025
Collection: Directory of Open Access Journals: DOAJ Articles
Subject Terms: Medicine
Description: Background Severe asthma is a heterogeneous airway inflammatory disease presenting with varying clinicophysiological characteristics and response to treatments. The objectives of the present study were to determine the clinical phenotypes of the Chinese C-BIOPRED cohort and their link to the sputum proteome. Methods Partition-around-medoids clustering was applied to a training set of 362 nonsmoking, smoking or ex-smoking severe asthma patients, and nonsmoking mild–moderate asthma patients using eight clinicophysiological variables, with validation performed in the remaining 181. Results Three stable clusters were defined, with Cluster T1 composed of predominantly female patients with severe nonsmoking asthma experiencing frequent exacerbations with moderate airflow obstruction, and Cluster T3 of elderly male patients with smoking/ex-smoking late-onset severe asthma and severe airflow obstruction and a moderate number of exacerbations. Cluster T2 was composed of nonsmokers with a mild–moderate airflow obstruction and no previous exacerbations. Validation clusters (V1, V2 and V3) were similar to the training set clusters. Differentially expressed proteins in sputum supernatants measured by liquid chromatography with tandem mass spectrometry pointed to differences in the complement and coagulation cascade pathway between Cluster 1 (T1 and V1) and Cluster 3 (T3 and V3), as well as between Cluster 2 (T2 and V2) and Cluster 3. Galectin 10 was upregulated in Cluster 1 compared with Cluster 2, and correlated with exacerbations, fractional exhaled nitric oxide, blood and sputum eosinophil count and oral corticosteroid dose in Cluster 1. Conclusion The clinical clusters were differentiated by smoking status, degree of airflow obstruction and exacerbation history, and by sputum complement and coagulation pathways, and galectin 10 levels.
Document Type: article in journal/newspaper
Language: English
Relation: http://openres.ersjournals.com/content/11/4/01016-2024.full; https://doaj.org/toc/2312-0541; https://doaj.org/article/ab2f62c0f4d249e18776c977c8d95a66
DOI: 10.1183/23120541.01016-2024
Availability: https://doi.org/10.1183/23120541.01016-2024; https://doaj.org/article/ab2f62c0f4d249e18776c977c8d95a66
Accession Number: edsbas.47F53660
Database: BASE