Julen N, Davrinche C, Ozanne D, Lebreton J P, Fontaine M, Ripoche J, Daveau M
INSERM Unité 78, Bois-Guillaume, France.
Mol Immunol. 1992 Jul-Aug;29(7-8):983-8. doi: 10.1016/0161-5890(92)90137-m.
The biosynthesis of alternative regulatory complement protein factor H was investigated using both an in vivo rat model and an in vitro rat hepatocyte culture system, and compared to that of C3 component. Subcutaneous injection of a single dose of 20 micrograms of recombinant murine tumor necrosis factor-alpha (rmTNF-alpha) had no effect on factor H liver mRNA levels, while it increased C3 mRNA levels. In correlation with this, serum factor H levels remained unchanged after rmTNF-alpha injection, whereas C3 levels were increased. In contrast in vitro studies showed that rmTNF-alpha had no effect on factor H and C3 expression by rat hepatocytes. Recombinant human interleukin-1 alpha (rhIL-1 alpha) did not alter the expression of factor H, whereas it increased C3 expression, and recombinant human interleukin-6 (rhIL-6) stimulated expression of both proteins. This study shows that TNF-alpha is not directly responsible for the increased levels of factor H observed in vivo during induced inflammation in the rat. Its in vivo effect on C3 secretion might be secondary to the TNF-alpha-induced release of IL-1 and/or IL-6.
利用体内大鼠模型和体外大鼠肝细胞培养系统研究了替代调节补体蛋白H因子的生物合成，并与C3成分进行了比较。皮下注射单剂量20微克重组鼠肿瘤坏死因子-α（rmTNF-α）对H因子肝脏mRNA水平没有影响，但增加了C3 mRNA水平。与此相关的是，注射rmTNF-α后血清H因子水平保持不变，而C3水平升高。相比之下，体外研究表明，rmTNF-α对大鼠肝细胞的H因子和C3表达没有影响。重组人白细胞介素-1α（rhIL-1α）不会改变H因子的表达，但会增加C3表达，而重组人白细胞介素-6（rhIL-6）会刺激这两种蛋白质的表达。这项研究表明，TNF-α并非大鼠诱导性炎症期间体内观察到的H因子水平升高的直接原因。其对C3分泌的体内作用可能继发于TNF-α诱导的IL-1和/或IL-6释放。
