Eosinophil peroxidase promotes bronchial epithelial cells to secrete asthma-related factors and induces the early stage of airway remodeling

Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 263(2024) vom: 22. Juni, Seite 110228
1. Verfasser: Xu, Liping (VerfasserIn)
Weitere Verfasser: Huang, Xuemei, Chen, Zhangrong, Yang, Meiling, Deng, Jingmin
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2024
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Airway remodeling Asthma Eosinophil peroxidase Epithelial-mesenchymal transition Inflammatory ADAM33 protein, human TSLP protein, human 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one IL5 protein, human TGFB1 protein, human
Beschreibung
Zusammenfassung:Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.
Asthma is a heterogeneous disease characterized by chronic airway inflammation, reversible airflow limitation, and airway remodeling. Eosinophil peroxidase (EPX) is the most abundant secondary granule protein unique to activated eosinophils. In this study, we aimed to illustrate the effect of EPX on the epithelial-mesenchymal transition (EMT) in BEAS-2B cells. Our research found that both EPX and ADAM33 were negatively correlated with FEV1/FVC and FEV1%pred, and positively correlated with IL-5 levels. Asthma patients had relatively higher levels of ADAM33 and EPX compared to the healthy control group. The expression of TSLP, TGF-β1 and ADAM33 in the EPX intervention group was significantly higher. Moreover, EPX could promote the proliferation, migration and EMT of BEAS-2B cells, and the effect of EPX on various factors was significantly improved by the PI3K inhibitor LY294002. The findings from this study could potentially offer a novel therapeutic target for addressing airway remodeling in bronchial asthma, particularly focusing on EMT
Beschreibung:Date Completed 17.05.2024
Date Revised 21.08.2024
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2024.110228