Tuberc Respir Dis > Volume 42(5); 1995 > Article
Tuberculosis and Respiratory Diseases 1995;42(5):703-712.
DOI: https://doi.org/10.4046/trd.1995.42.5.703    Published online October 1, 1995.
Study on IL-8 Expression in Peripheral Blood Monocytes.
Jae Yeol Kim, Jae Cheol Lee, Min Jong Kang, Jae Seok Park, Chul Gyu Yoo, Young Whan Kim, Sung Koo Han, Young Soo Shim
1Department of Internal Medicine and Tuberculosis Research Institute, Seoul National University College of Medicine, Seoul, Korea.
2Deaprtment of Internal Medicine, Seoul City Boramae Hospital, Seoul, Korea.
Abstract
BACKGROUND
Peripheral blood monocytes are important immune effector cells that play a fundamental role in cellular immunity. In addition to their antigen-presenting and phagocytic activities, monocytes/macrophage produce a vast array of regulatory and chemotactic cytokines. Interleukin-8(IL-8), a potent neutrophil-activating and chemotactic peptide, is produced in large quantities by mononuclear phagocytes and may be an important mediator of local and systemic inflammation. Overexpression by IL-8 of such inflammation may be an important step of tissue injury frequently seen in inflammatory reaction. So it could be hypothesized that the agents which block the production of IL-8 can decrease the inflammatory reaction and tissue injury. To evaluate this, we described the effect of Dexamethasone, PGE2, Indomethacin and Interferon-gamma(IFN-gamma) on IL-8 mRNA and protein expression from LPS-stimulated human peripheral blood monocytes (PBMC). METHOD: PBMC was isolated from healthy volunteers. To evaluate the effect of Dexamethasone, PGE2 & Indomethacin, these drug were treated for 1 hour before and after LPS stimulation and IFN-gamma was only treated 1 hour before the LPS stimulation. Northern blot analysis for IL-8 mRNA and ELISA for immunoreactive IL-8 protein in culture supernatant were performed. We repeated above experiment three times for Northern blot analysis and two times for ELISA and got the same result. RESULTS: 1) Pre- and post-treatment of Dexamethasone suppressed both the LPS stimulated IL-8 mRNA expression and IL-8 protein release in PBMC. 2) IFN-gamma pre-treatment suppressed the IL-8 mRNA expression and IL-8 protein release in unstimulated cells. 3) In LPS stimulated cells, IFN-gamma suppressed the IL-8 mRNA expression but IL-8 protein release suppression was not observed. 4) PGE2 and Indomethacin exert no effect on the LPS-stimulated IL-8 mRNA and protein expression in concentration used in this experiment (PGE2;10 6M, Indomethacin; l0microM). CONCLUSION: One of the mechanism of antiinflammatory action of Dexamethasone can be explained by the suppressing effect of IL-8 production in some extent and by this antiinflammatory effect, dexamethasone can be used to suppress local and systemic inflammation mediated by IL-8.
Key Words: LPS, IL-8, PBMC, Dexamethasone, PGE2, Indomethacin, Interferon-gamma


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