| First Author | Marchant A | Year | 1996 |
| Journal | Clin Exp Immunol | Volume | 106 |
| Issue | 1 | Pages | 91-6 |
| PubMed ID | 8870704 | Mgi Jnum | J:35618 |
| Mgi Id | MGI:83065 | Doi | 10.1046/j.1365-2249.1996.d01-799.x |
| Citation | Marchant A, et al. (1996) Methylprednisolone differentially regulates IL-10 and tumour necrosis factor (TNF) production during murine endotoxaemia. Clin Exp Immunol 106(1):91-6 |
| abstractText | 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. |
