Open AccessMethylprednisolone differentially regulates IL‐10 and tumour necrosis factor (TNF) production during murine endotoxaemia
Author(s) -
MARCHANT A.,
AMRAOUI Z.,
GUEYDAN C.,
BRUYNS C.,
LE MOINE O.,
VANDENABEELE P.,
FIERS W.,
BUURMAN W. A.,
GOLDMAN M.
Publication year - 1996
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1046/j.1365-2249.1996.d01-799.x
Subject(s) - methylprednisolone , tumor necrosis factor alpha , immunology , tumor necrosis factor α , necrosis , medicine , cytokine , corticosteroid , biology
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 μg/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.