Factors associated with plasma IL-33 levels in patients with chronic obstructive pulmonary diseaseopen access
- Authors
- Kim, Sei Won; Rhee, Chin Kook; Kim, Ki Uk; Lee, Sang Haak; Hwang, Hun Gyu; Kim, Yu Il; Kim, Deog Kyeom; Do Lee, Sang; Oh, Yeon-Mok; Yoon, Hyoung Kyu
- Issue Date
- 2017
- Publisher
- Dove Medical Press Ltd
- Keywords
- biomarker; cytokine; interleukin-33; eosinophil; pathogenesis; chronic bronchitis
- Citation
- International Journal of COPD, v.12, pp 395 - 402
- Pages
- 8
- Journal Title
- International Journal of COPD
- Volume
- 12
- Start Page
- 395
- End Page
- 402
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/8391
- DOI
- 10.2147/COPD.S120445
- ISSN
- 1176-9106
1178-2005
- Abstract
- Background: Interleukin (IL)-33 promotes T helper (Th)2 immunity and systemic inflammation. The role of IL-33 in asthma has been widely investigated. IL-33 has also been suggested to play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). This study investigated the clinical significance and usefulness of plasma IL-33 level in patients with COPD. Methods: A total of 307 patients with stable COPD from 15 centers, who were in the Korean Obstructive Lung Disease cohort, were enrolled in this study. Plasma IL-33 levels were measured by enzyme-linked immunosorbent assay. We analyzed the association between IL-33 level and other clinical characteristics related to COPD. We also examined the features of patients with COPD who exhibited high IL-33 levels. Results: IL-33 levels varied, but were very low in most patients. Eosinophil count was significantly correlated with a plasma IL-33 level. In addition, old age and current smoking were related to a low IL-33 level. Significantly more patients with a higher IL-33 level had chronic bronchitis compared with those with a low IL-33 level. Conclusion: Plasma IL-33 level in patients with stable COPD was related to eosinophil count and chronic bronchitis phenotype. Further studies are needed to identify the precise mechanisms of IL-33/ST2 pathway in patients with COPD.
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