Abstract.
Objective: Interleukin (IL)-18 is involved in host defense mechanisms and inflammatory diseases, among them rheumatoid arthritis (RA). High levels of IL-18 expression in RA joints are contrasted by reduced IL-18 expression in RA peripheral blood mononuclear cells (PBMC). Here, we investigated a putative IL-18 regulating role of corticosteroids.¶Methods: IL-18 transcript and protein levels in PBMC from untreated and prednisolone treated RA patients, and from healthy donors were assessed by semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR) and immunoblotting. IL-18 regulation was determined in PBMC and U937 cells upon exposure to prednisolone in vitro by RT-PCR and Northern Blot analysis, by ELISA in cell culture supernatants, and in transiently transfected THP-1 cells by IL-18 promoter activity luciferase assays.¶Results: In RA PBMC, IL-18 transcript levels were dose dependently restored, in parallel with administered prednisolone treatment, to subnormal levels. The corresponding intracellular IL-18 deposits in contrast were depleted. In cultured PBMC and promonocytic cell lines, prednisolone up-regulated IL-18 transcription in parallel with increasing the IL-18 protein release into cell culture supernatants.¶Conclusion: Prednisolone increases IL-18 expression and release in PBMC and monocytic cell lines.
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Received 24 January 2002; returned for revision 7 March 2002; accepted by G. Geisslinger 15 May 2002
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Möller, B., Kukoc-Zivojnov, N., Koyama, N. et al. Prednisolone induces interleukin-18 expression in mononuclear blood and myeloid progenitor cells. Inflamm. res. 51, 457–463 (2002). https://doi.org/10.1007/PL00012412
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DOI: https://doi.org/10.1007/PL00012412