Methylprednisolone differentially regulates IL-10 and tumour necrosis factor (TNF) production during murine endotoxaemia

A. Marchant, Z. Amraoui, C. Gueydan, C. Bruyns, O. Lemoine, P. Vandenabeele, W. Fiers, W.A. Buurman, M. Goldman

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Methylprednisolone differentially regulates IL-10 and tumour necrosis factor (TNF) production during murine endotoxaemia.

Marchant A, Amraoui Z, Gueydan C, Bruyns C, Le Moine O, Vandenabeele P, Fiers W, Buurman WA, Goldman M.

Laboratoire d'immunologie Experimentale, Universite Libre de Bruxelles, Belgium.

IL-10 is an endogenous antiinflammatory cytokine that inhibits TNF biosynthesis and protects mice from lipopolysaccharide (LPS)-induced lethality. As synthetic glucocorticoids are widely used as antiinflammatory agents, we analysed the effects of methylprednisolone administration on IL-10 biosynthesis during murine endotoxaemia. We found that low doses of methylprednisolone (2-10 mg/kg) markedly inhibited TNF production but did not affect serum levels of IL-10, while a high methylprednisolone dose (50 mg/kg) increased LPS-induced IL-10 levels. In parallel, we observed that LPS-induced IL-10 production is TNF-independent in this experimental setting. Experiments conducted in vitro indicated that methylprednisolone (from 0.01 to 100 micrograms/ml) also increased the biosynthesis of IL-10 by LPS-activated mouse peritoneal macrophages. We conclude that methylprednisolone differentially regulates IL-10 and TNF production induced by LPS both in vivo and in vitro at the macrophage level.
Original languageEnglish
Pages (from-to)91-96
JournalClinical and Experimental Immunology
Volume106
DOIs
Publication statusPublished - 1 Jan 1996

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