Lipofundin Mediates the Major Inhibition of Intravenous Propofol in IL-1β Secretion and Phagocytosis of Staphylococcus aureus-Infected Macrophages.

Lipofundin is the solvent for propofol in the intravenous injection of Propofol-Lipuro (R) and is used in patients who need intravenous feeding to provide fatty acids and fat for energy. In addition to propofol, Lipofundin also affects the immune modulation of phagocytes. In a previous study, we reported that intravenous propofol effectively decreased Staphylococcus aureus-stimulated reactive oxygen species (ROS) levels, IL-1 beta secretion, and phagocytosis in RAW264.7 macrophages. It is important to separately assess the effects of pure propofol, Lipofundin, and Propofol-Lipuro. By using an S. aureus-infected RAW264.7 macrophage model, the levels of secreted IL-1 beta in cell supernatants were determined by ELISA. IL-1 beta mRNA in cell pellets was further analyzed by quantitative polymerase chain reaction (qPCR), and Western blotting was performed to detect pro-IL-1 beta synthesis. Total ROS levels were determined by a luminol chemiluminescence assay. Compared with pure propofol, treatment with clinically relevant concentrations of Propofol-Lipuro and Lipofundin obviously reduced IL-1 beta secretion (>85% inhibition), S. aureus-stimulated ROS production (50% inhibition), and phagocytosis (>60% inhibition) to similar levels. Treatment with pure propofol alone significantly decreased IL-1 beta mRNA levels and pro-IL-1 beta protein synthesis, and slightly inhibited phagocytosis. In contrast, treatment with Propofol-Lipuro did not influence IL-1 beta mRNA or pro-IL-1 beta protein expression, even though treatment with Lipofundin increased the levels of both IL-1 beta mRNA and its precursor protein. In conclusion, IL-1 beta secretion is regulated at the posttranslational level. Lipofundin mediated the major effect of Propofol-Lipuro on the inhibition of IL-1 beta secretion, ROS production, and phagocytosis in S. aureus-infected RAW264.7 cells.