IL-1Ra elaboration by colchicine stimulation in normal human bronchial epithelial cells
- Authors
- Lee, Jae Hyung; Kim, Sang Heon; Kim, Tae Hyung; Sohn, Jang Won; Yoon, Ho Joo; Shin, Dong Ho; Park, Sung Soo
- Issue Date
- Aug-2007
- Publisher
- Korean National Tuberculosis Association
- Keywords
- Asthma; Colchicine; IL-1Ra; MAPK
- Citation
- Tuberculosis and Respiratory Diseases, v.63, no.2, pp.145 - 153
- Indexed
- SCOPUS
KCI
- Journal Title
- Tuberculosis and Respiratory Diseases
- Volume
- 63
- Number
- 2
- Start Page
- 145
- End Page
- 153
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/179752
- DOI
- 10.4046/trd.2007.63.2.145
- ISSN
- 1738-3536
- Abstract
- Background: Asthma is a syndrome that is characterized by a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation Colchicine is an inexpensive and safe medication with unique anti-inflammatory properties. IL-1Ra (Interleukin-1 receptor antagonist) mediates the anti-inflammatory effect in human inflammatory diseases, including asthma. This study examined whether IL-1Ra mediates the anti-inflammatory effect of colchicine in normal human bronchial epithelial cells (NHBE), RAW 264.7 cells (murine macrophage cell line), and a mouse lung. Methods: NHBE, RAW 264.7 cells and BALB/c mice were stimulated with colchicine, and the increase in the IL-1Ra level was estimated by ELISA, Western analysis and RT-PCR analysis. Results: Colchicine stimulated NHBE and RAW 264.7 cells to release IL-1Ra into the supernatant in a dose-and time-dependent manner. The major isoform of IL-1Ra in NHBE and RAW 264.7 cells is type I icIL-1Ra, and sIL-1Ra, respectively. IL-1Ra up-regulation was blocked by PD98059, a specific inhibitor in MAPK pathways. Colchicine also stimulated the secretion of IL-1Ra into the bronchoalveolar lavage (BAL) fluid of BALB/c mouse. Conclusion: Colchicine stimulates an increase in the IL-1Ra level both in vivo and in vitro, and might have an anti-inflammatory effect.
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