par Marchant, Arnaud 
;Amraoui, Z;Gueydan, Cyril ;Bruyns, C;Le Moine, Olivier ;Vandenabeele, P;Fiers, Walter;Buurman, Wim;Goldman, Michel
Référence Clinical and experimental immunology, 106, 1, page (91-96)
Publication Publié, 1996-10
;Amraoui, Z;Gueydan, Cyril ;Bruyns, C;Le Moine, Olivier ;Vandenabeele, P;Fiers, Walter;Buurman, Wim;Goldman, Michel Référence Clinical and experimental immunology, 106, 1, page (91-96)
Publication Publié, 1996-10
Article révisé par les pairs
| Résumé : | 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. |
