Augmentation of glucocorticoid action on human monocytes by interleukin-4

P. H. Hart, G. A. Whitty, D. R. Burgess, M. Croatto, J. A. Hamilton

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43 Citations (Scopus)


For their anti-inflammatory effects, glucocorticoids act, at least in part, by suppression of the production of interleukin-1 (IL-1), tumor necrosis factor α (TNFα) and prostaglandin E2 (PGE2) by activated monocytes/macrophages. Interleukin-4 (IL-4) also suppresses similar parameters of monocyte activation in vitro. However, contrasting effects of IL-4 and dexamethasone (Dex) on monocyte tissue-type plasminogen activator (t-PA) production suggest that these agents may operate by different pathways. We have now demonstrated that levels of IL-4 as low as 0.05-0.1 U/ml (0.6-1.2x10-11M) can augment the actions of Dex (5x10-9M) as an inhibitor of the production of monocyte pro-inflammatory mediators. These in vitro results suggest the possible supplementation of steroid therapy with low amounts of IL-4 (or an agonist) permitting the use of less steroid with concomitant reduction in steroid-associated side-effects. IL-4 can also suppress the increased release of IL-1β and TNFα by monocytes incubated with indomethacin, a non-steroidal anti-inflammatory drug.

Original languageEnglish
Pages (from-to)147-153
Number of pages7
JournalLymphokine Research
Issue number2
Publication statusPublished - 1 Jan 1990
Externally publishedYes


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