| IL-1Ra Elaboration by Colchicine Stimulation in Normal Human Bronchial Epithelial Cells. |
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Jae Hyung Lee, Sang Heon Kim, Tae Hyung Kim, Jang Won Sohn, Ho Joo Yoon, Dong Ho Shin, Sung Soo Park |
1Department of Internal Medicine, Eulji General Hospital, Eulji University School of Medicine, Seoul, Korea.
2Department of Internal Medicine, College of Medicine, Hanyang University, Seoul, Korea. parkss@hanyang.ac.kr |
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| 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. |
| Key Words:
Colchicine, Asthma, IL-1Ra, MAPK |
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