Potential antiinflammatory effects of interleukin 4: Suppression of human monocyte tumor necrosis factor α, interleukin 1, and prostagandin E₂

Stimulated human monocytes/macrophages are a source of mediators such as tumor necrosis factor α (TNF-α), interleukin 1 (IL-1), and prostaglandin E₂ (PGE₂), which can modulate inflammatory and immune reactions. Therefore, the ability to control the production of such mediators by monocytes/macrophages may have therapeutic benefits, and its has been proposed that glucocorticoids may act in this way. Purified human monocytes, when stimulated in vitro with lipopolysaccharide (LPS) or with LPS and γ interferon (IFN-γ), produce TNF-α, IL-1, and PGE₂. Cotreatment of stimulated cells with the purified human lymphokine, interleukin 4 (IL-4 ≥ 0.1-0.5 unit/ml; 12-60 pM) dramatically blocked the increased levels of these three mediators; for TNF-α and IL-1, the inhibition was manifest at the level of mRNA. Thus, IL-4 can suppress some parameters of monocyte activation and, as for B cells, have opposite effects to IFN-γ. The effects of IL-4 on human monocytes are similar to those obtained with the glucocorticoid dexamethasone (0.1 μM).