Cytokine regulation of human monocyte interleukin‐1 (IL‐1) production in vitro. Enhancement of IL‐1 production by interferon (IFN) gamma, tumour necrosis factor‐alpha, IL‐2 and IL‐1, and inhibition by IFN‐alpha

• Published in: Clinical and experimental immunology Vol. 80; no. 3; pp. 435 - 443
• Main Authors: DANIS, V. A., KULESZ, A. J., NELSON, D. S., BROOKS, P. M.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.06.1990
• Subjects: Biological Factors - immunology; Biological Factors - pharmacology; Cells, Cultured; Cytokines; Humans; In Vitro Techniques; inteferons; Interferon Type I - immunology; Interferon-gamma - immunology; Interleukin-1 - biosynthesis; Interleukin-1 - immunology; Interleukin-2 - immunology; interleukin‐1; interleukin‐2; monocytes; Monocytes - immunology; Monocytes - metabolism; Recombinant Proteins; Tumor Necrosis Factor-alpha - immunology; tumour necrosis factor‐alpha
• ISSN: 0009-9104; 1365-2249
• DOI: 10.1111/j.1365-2249.1990.tb03306.x

SUMMARY IL‐1 production (secreted and cell‐associated) was measured in monocyte cultures stimulated by a variety of agents in vitro. Monocytes either adherent to conventional plastic culture plates in serum‐free conditions, or in suspension in culture medium containing serum were stimulated to produce IL‐1 during culture. In non‐adherent, serum‐free conditions, monocytes produced very low or undetectable amounts of IL‐1 during 20 h of culture. Lipopolysaccharide (LPS) induced equivalent amounts of secreted and cell‐associated IL‐1, although at very low concentrations more cell‐associated IL‐1 was produced. IL‐1 production in response to LPS could be augmented by crude lymphokine, IFN‐γ, or tumour necrosis factor (TNF) alpha. TNF‐α preferentially augmented the production of cell‐associated IL‐1 in LPS‐stimulated cultures. TNF‐α induced a significant amount of IL‐1 (mainly cell‐associated) directly but could also induce IL‐1 secretion when combined with IL‐2 or IFN‐γ, or when in the presence of serum. IL‐2 acted synergislically with low concentrations of IFN‐γ or IL‐1 to induce significant levels of IL‐1 production. IFN‐α did not induce any IL‐1 production, but was a potent inhibitor of IL‐1 production induced by a variety of stimuli. These results suggest that IL‐1 production may be enhanced or reduced by different cytokines at concentrations likely to be found in chronic inflammatory lesions.