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Association of interleukin-25 levels with development of aspirin induced respiratory diseases
- 작성일2018-02-14
- 최종수정일2018-02-14
- 담당부서연구기획과
- 연락처043-719-8033
- 3,129
Respiratory Medicine, 2017, 01, 71─78, DOI: https://doi.org/10.1016/j.rmed.2016.11.020.
Association of interleukin-25 levels with development of aspirin induced respiratory diseases
Jong-Uk Lee, HJ Lee;DJ Bae;JH Son;JS Park;JS Choi;HG Hwang;CS Park
Abstract
Background
Aspirin-exacerbated respiratory diseases (AERD) are caused by ingestion of non-steroidal anti-inflammatory drugs and are characterized by acute bronchospasms and marked infiltration of eosinophils, the latter being attributable to altered synthesis of cysteinyl leukotrienes (LT) and prostaglandins (PG). Recently, the innate Th2 response is revealed to induce eosinophil infiltration in allergic inflammation, however the role of the innate Th2 response has not been studies in AERD. Thus, we evaluated the relationship between the innate Th2 cytokines including IL-25, thymic stromal lymphopoietin(TSLP) and IL-33 and the development of AERD.
Methods and materials
Plasma IL-25, IL-33, and TSLP levels were measured before and after aspirin challenge in subjects with AERD (n ¼ 25) and aspirin-tolerant asthma (ATA, n ¼ 25) by enzyme-linked immunosorbent assay (ELISA). Pre and post-aspirin challenge levels of LTC4 and PGD2 were measured using ELISA.
Results
Basal plasma IL-25 levels were significantly higher in AERD group than in normal controls and in ATA group (p ¼ 0.025 and 0.031, respectively). IL-33 and TSLP levels were comparable in the AERD and ATA groups. After the aspirin challenge, the IL-25 levels were markedly decreased in the ATA group (p ¼ 0.024), while not changed in the AERD group. The post-challenge IL-25 levels of all asthmatic subjects were significantly correlated with aspirin challenge - induced declines in FEV1 (r ¼ 0.357, p ¼ 0.011), but not with basal and post challenge LTC4 and PGD2 levels.
Conclusions
IL-25 is associated with bronchospasm after aspirin challenge, possibly via mechanisms other than altered LTC4 and PGD2 production.
- DOI: https://doi.org/10.1016/j.rmed.2016.11.020.
- ISBN or ISSN: 0954-6111
- 본 연구는 질병관리본부 연구개발과제(과제번호 2017-보건의료생물자원종합관리) 연구비를 지원받아 수행되었습니다.
- This research was supported by a fund(code 2017-보건의료생물자원종합관리) by Research of Korea Centers for Disease Control and Prevention.
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