ArticleBiomolecules2024
Serum T2-High Inflammation Mediators in Eosinophilic COPD.
Article in Biomolecules, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Beyond Eosinophil Depletion: IL-5 as a Context-Dependent Regulator of Airway Immune Networks.International journal of molecular sciences · 2026Review
- Review
- GLP-1RAs: antidiabetic drug crossover-new hope for chronic inflammatory airway diseases.Respiratory research · 2026Review
- Real-World Identification of Eosinophilic COPD Patients Potentially Eligible for Dupilumab: A Retrospective Observational Study.International journal of chronic obstructive pulmonary disease · 2026Observational
- Multi-Criteria Decision Analysis of Biologics in Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
Eosinophils are central inflammatory cells in asthma; however, a portion of patients with chronic obstructive pulmonary disease (COPD) have blood or sputum eosinophilia, a condition termed eosinophilic COPD (eCOPD), which may contribute to the progression of the disease. We hypothesize that eosinophilic inflammation in eCOPD patients is related to Type 2 (T2)-high inflammation seen in asthma and that serum mediators might help us to identify T2-high inflammation in patients and choose an appropriate personalized treatment strategy. Thus, we aimed to investigate ten serum levels of T2-high inflammation mediators in eCOPD patients and compare them to severe non-allergic eosinophilic asthma (SNEA) patients. We included 8 subjects with eCOPD, 10 with SNEA, and 11 healthy subjects (HS) as a control group. The concentrations of biomarkers in serum samples were analyzed using an enzyme-linked immunosorbent assay (ELISA). In this study, we found that eCOPD patients were distinguished from SNEA patients by elevated serum levels of sIL-5Rα, MET, TRX1, ICTP, and IL-4, as well as decreased serum levels of eotaxin-1 and sFcεRI. Moreover, MET, ICTP, eotaxin-1, and sFcεRI demonstrated high sensitivity and specificity as potential biomarkers for eCOPD patients. Furthermore, serum levels of IL-5 and IL-25 in combination with sIL-5Rα, MET, and IL-4 demonstrated a high value in identifying T2-high inflammation in eCOPD patients. In conclusion, this study highlights that while T2-high inflammation drives eosinophilic inflammation in both eCOPD and SNEA through similar mechanisms, the distinct expression of its mediators reflects an imbalance between T1 and T2 inflammation pathways in eCOPD patients. A combined analysis of serum mediators may aid in identifying T2-high inflammation in eCOPD patients and in selecting an appropriate personalized treatment strategy.
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