Kupffer cell complement receptor clearance function after surgical injury and phagocytosis of immune complexes: effect of changes in plasma fibronectin.

Abstract

The present study evaluated the effect of changes in plasma fibronectin levels on the degree of depression of in vivo clearance function of Kupffer cell complement receptors after injury and the phagocytosis of immune complexes. In vitro studies have suggested that fibronectin may act as an opsonin for the clearance of immune complexes from the blood by binding to C1q and may influence the expression and activation of immune receptors on macrophages. Complement receptor clearance function was assessed in rats from the hepatic uptake of rat erythrocytes coated with antierythrocyte IgM. Increasing plasma fibronectin by the injection of purified fibronectin or decreasing fibronectin by the injection of gelatin had no effect on complement receptor function in otherwise normal animals. Surgical injury depressed both plasma fibronectin levels and complement receptor function. Injection of fibronectin at the time of injury prevented the depression of receptor function; however, when fibronectin was given 1 hour after injury, receptor function remained depressed even though fibronectin levels were increased. The phagocytosis of immune complexes (IgG-coated rat erythrocytes [EIgGs]) depressed complement receptor function but did not depress plasma fibronectin levels. The depression of receptor function caused by the phagocytosis of EIgGs was prevented by administering fibronectin and was potentiated by administering gelatin, which decreased plasma fibronectin levels. Therefore, plasma fibronectin concentrations can influence in vivo Kupffer cell complement receptor function under certain conditions that lead to the depression of complement receptor function.